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BIOCHEMISTRY
QUICK REVISION NOTES

CONCEPTS to give 3 fatty acids and glycerol.

•• Fatty acid and Glycerol are smaller molecules,
Basics so they enter adipose tissues.
•• Fed: Within 2 hours of food intake •• In adipose tissues, they rejoin to form TGs
•• Fasting: 12-18 hours period (lack of food) again, which are stored here (anabolic role).
•• Starvation (prolonged fasting): 1-3 days (lack of Hormone Sensitive Lipase (HSL)
food)
•• This enzyme is present inside the cells of
Smile Formula-1 adipose tissues
•• Stored triglycerides in adipose tissues are
Anabolic Pathways List broken by HSL into 3 fatty acids and glycerol
•• Glycogenesis (synthesis of glycogen)
•• 3 fatty acid go in blood and then taken by liver
•• HMP (synthesis of Ribose-5-P & NADPH) where β- Oxidation of fatty acids (catabolic)
occurs to give energy in Liver.
•• Fatty Acid Synthesis
•• Triglyceride Synthesis Synthesis of fat (lipogenesis)

•• Cholesterol Synthesis
Smile Formula 2
•• Insulin acts in Fed state, so is always an anabolic
•• Enzyme: Lipoprotein LipaseQ
hormone
Catabolic Pathways List •• Glucagon acts in fasting/starvation state, so is
•• Glycolysis (breakdown of glucose to pyruvate) a catabolic hormone

•• Link reaction by PDH complex [Pyruvate (3C) → •• Insulin activates all anabolic pathwaysQ
Acetyl CoA (2C)] –– Exception: Insulin also activates 2 catabolic
•• Glycogenolysis (breakdown of glycogen) pathways:

•• β- Oxidation of fatty acids (breakdown of fatty 1. Glycolysis

acid) 2. Link Reaction
•• Gluconeogenesis (occurs in fasting/starvation •• Glucagon activates all catabolic pathways
state as something is broken down for making
–– But it will not activate two catabolic pathways:
glucose)
glycolysis and link reaction
•• Ketone body synthesis (fats broken down to
form KB) Phosphorylation and Dephosphorylation
•• Ketone body utilization
•• Enzyme: Hormone sensitive lipase (HSL)Q

Lipoprotein Lipase (LPL)

This enzyme is present in endothelium of blood vessels
•• Lipoprotein lipase enzyme breaks triglycerides
(TGs) of Lipoproteins (Chylomicrons and VLDL)
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Biochemistry

•• Insulin always ↓cAMP and causes Sources Of Blood Glucose

DephosphorylationQ
1.Food
–– Insulin activate phosphodiesterase
2. Liver Glycogen (provides blood glucose for 12-18 hours)
–– Lack of cAMP causes dephosphorylation
3. Gluconeogenesis
•• Glucagon always ↑cAMP and causes
Phosphorylation Note: Never answer fats for above question

–– Glucagon activate adenyl cyclase thereby Preferred/Main fuel for body

synthesizing cAMP from ATP
•• 1st is carbohydrates
–– cAMP causes phosphorylation
•• 2nd is fats
Smile Formula 3 •• 3rd is amino acids/proteins
•• The pathways/enzyme which are activated by Important Information
insulin (All anabolic pathways + Glycolysis & Link
reaction) are always active in dephosphorylated •• Fats can never by converted to carbohydrates
state as link reaction is irreversible

•• The pathways/ enzyme which are activated by Exception: Two breakdown products of fats can be
glucagon are always active in phosphorylated converted to glucose:Q
state 1. Glycerol → Break down product of TG

Smile Formula 4 2. Propionic acid → obtained from Break down

product of Odd chain F.A
Which pathway occurs in which compartment of the
cell?
•• All catabolic pathways occur in Mitochondria
•• All anabolic pathways occur in cytoplasm
–– Exception: Glycolysis and Glycogenolysis
(Catabolic pathways BUT occurs in Cytoplasm)
Three pathways occur in both Mitochondria &
CytoplasmQ
1. Urea cycle
2. Heme synthesis
3. Gluconeogenesis
Note: Start (first enzymatic reaction) of these 3
pathways occurs in mitochondria
CYTOPLASM MITOCHONDRIA
HMP Beta oxidation of fatty acids,
Link reaction
Glycogenesis Apoptosis
FA synthesis Ketone body synthesis &
Ketone body utilization
Cholesterol synthesis Vital pathways -TCA & ETC
Exceptions – Glycolysis, Replication, Transcription,
Glycogenolysis Translation (for mitochondrial
DNA)
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Scene in fasting state 2. Acetyl CoA not available as it is diverted to KB synthesis,

3. NAD not available as it is used in beta oxidation.

FUELS FOR BODY IN VARIOUS STATES

Fed Fasting Starvation
Glucose
Brain Glucose (as F.A can’t Ketone bodies
cross B.B.B)
Heart Fatty acids Fatty acids Ketone bodies
Amino acid/
Liver Glucose Fatty acids
protein
Muscle Glucose Fatty acids FA, KB and AA
Adipose
Glucose Fatty acids Fatty acids
Tissue
Glucose
Glucose
Important Information (As no
As no
•• Acetyl CoA only activates first step of RBC Glucose mitochondria
mitochondria,
gluconeogenesis but can never be converted to For F.A
Can’t use K.B]
glucose. It is never glucogenic.Q utilization)

Diabetes Important Information

•• Decreased or absent Insulin •• Heart uses fatty acid in fed state.
•• Glucose is not able to go to peripheral tissues –– Fetal Heart: Fuel is glucose
& cells
–– Heart Failure: Fuel is glucose
•• So, it is same state as fasting/starvation
•• RBC always uses glucose [Any state]
•• So catabolic pathways will be activated, and
anabolic pathways will be deactivated. Basics Of Diet
Catabolic pathways ↑ Anabolic pathways ↓ •• Diet
HSL –– 60-70% carbohydrates
Lipolysis
–– 15-20% fats
β- oxidation of FA Lipoprotein lipase
–– Rest is proteins
Gluconeogenesis
KB Synthesis •• Only 50% of carbohydrates consumed, are used
to give energy, Rest 50% is stored:
Important Information
→ 10 % as glycogen
•• Only one anabolic thing happens in liver of
chronic diabetic patients → 40% is converted into fats known as
endogenous fats as formed inside body. They
–– There will be excess of acetyl CoA in liver
get transported as VLDL lipoprotein
(due to increased β- oxidation)
•• 15-20 % fat taken in diet is exogenous fat
→ This excess Acetyl CoA is forced to be
and is transported in the form of Chylomicron
used in Endogenous fatty acid synthesis lipoprotein.
and triglyceride synthesis (↑VLDL in lipid
Q. A person on fat free, carbohydrate rich diet
profile) and also Cholesterol synthesis
continuous to grow obese. Which lipoprotein is
TCA suppression occurs in DM because: increased?
1. Oxaloacetate not available as it is diverted to Ans. Excess carbohydrates get converted to fat
gluconeogenesis, inside body k/a endogenous fat causing weight gain.
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Biochemistry

Endogenous fat/TGs are transported in the form of

VLDL lipoproteins in blood.
Important Information
•• Atkin’s Diet – is for weight reduction- Low calorie,
Low carbohydrate diet
•• Fructose is the most lipogenic sugar

Thermogenic/Thermic effect of food/

SDA (specific dynamic action)
SDA: Amount of energy required to digest, absorb, Important Information
transport & metabolize food in body.
•• NADPH Involved in Reductive biosynthesis- in
•• It is maximum for Proteins > Carbohydrates > anabolic pathways
Fats.Q
•• NADH & FADH2 in Catabolic pathways
Enzyme Classification NADPH
•• 6 categories / Enzyme commission numbers /
Synthesized fromQ
Enzyme E.C number / Enzyme code numbers
1. HMP (Main Source)
•• Mnemonic: OTHLIL
2. Malic enzyme (Minor source)
Oxidoreductases Oxidation/Reduction reactions
Transfer of group from one molecule 3.Cytoplasm Isocitrate dehydrogenase (Minor Source)
Transferases
to other (Molecular formula changed) Note: All 3 enzymes lie in cytoplasm
Hydrolases Breaks bond using H2O
Enzyme Function EC No.
Make/Break a bond without H2O &
Lyases Dehydrogenase Does oxidation 1
ATP
Reductase Does reduction 1
Interconverts one isomer to other
Isomerases Transfer organic Phosphate
(Molecular formula remains same) Kinases 2
from ADP or ATP
Ligases Uses ATP to make the bond
Phosphorylase Transfer inorganic /free (Pi): 2
Phosphatase Removes PO4 using H2O 3

Important Information
Substrate Level Oxidative Phosphorylation/
•• Additional of O2 → Oxidation
Phosphorylation ETC
•• Addition of H2 or e- → Reduction In Glycolysis & TCA by Many oxidoreductases
•• H2/H atom/reducing equivalent = e- enzyme Kinase enzymes & ATP synthase

•• H+ ion → Proton ATP formed in only one Lot of steps

step
Gives only few ATPs in Gives most ATPs in the cells
Dehydrogenase
the cells
Causes removal of H2 i.e., some compounds are getting
oxidized. Synthesis
•• Synthase
–– ATP not used
–– E.C No = 4 (lyase)
•• Synthetase
–– ATP used
–– E.C No = 6 (ligase)
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All Synthase Are Lyases Except: Cell Organelle Marker

Enzyme EC No. •• Plasma Membrane •• Na+ K+ ATPase, 5’

Nucleotidase, Adenyl Cyclase
Nitric oxide synthase 1
•• Golgi Apparatus •• Galactosyl Transferase
Citrate synthase 2
•• Cytosol •• Lactate DH
Glycogen synthase 2
•• Ribosome •• rRNA
ATP synthase 3 •• ER •• Glucose-6-Phosphatase
•• Peroxisomes •• Catalase
Carboxylase •• Nucleus •• DNA, DNA Polymerase

•• Addition of CO2 to a molecule •• Mitochondria •• Succinate DH, Glutamate DH

•• Requires ABC (Mnemonic) Q

•• Lysosome •• Acid Phosphatase
–– A - ATP
–– B - Biotin / Vit B7 PREVIOUS YEAR QUESTIONS
–– C - CO2 Q. Cause of formation of ketone bodies in Diabetic
Ketoacidosis are all EXCEPT: (JIPMER Dec 2019)
•• Also ‘Mg’ is required for all the carboxylases
A. Acetyl CoA not participating in TCA Cycle
•• E.C. Number = 6 (Ligase category)
B. Increased activity of beta hydroxy butyrate
Decarboxylation (removal of CO2) dehydrogenase
C. Mobilization of fats from adipose tissue
1. Oxidative
D. Decreased fatty acid Oxidation
•• Requires Vit B1 as co-enzyme
Exp: There is increased beta oxidation of Fatty acids
•• E.C No = 1 due to higher fat mobilization from adipose tissues.
•• Enzyme used: Dehydrogenase i.e., Removal of
Q. K e t o n e b o d i e s a r e n o t u t i l i z e d b y ?
CO2 along with oxidation.
(JIPMER Dec 2019)
2. Simple A. Brain
•• Requires Vit B6 as co-enzyme B. RBC
C. Heart
•• E.C No = 4
D. Skeletal muscle
•• Here CO2 removed without use of H2O (Lyase
category) Exp: RBCs lack mitochondria and, therefore, cannot
utilize ketone bodies as a source of energy

Q. In case of Lipoprotein Lipase (LPL) deficiency,

which of the following will increase after a fat rich
diet? (NEET Jan 2019)
ExamplesQ A. Chylomicron

1. Histidine → Histamine B. HDL

C. Lipoprotein (a)
2. Tryptophan → Tryptamine
D. LDL
3. Tyrosine → Tyramine
Exp: LPL deficiency impairs the hydrolysis of triglycerides
4. DOPA → Dopamine in chylomicrons and VLDL, leading to elevated levels of
5. Serine → ethanolamine chylomicrons and VLDL, after a fat-rich diet.

6. Cysteine → β-mercaptoethanolamine Q. Enzyme activated by decrease in Insulin: Glucagon

ratio? (NEET Jan 2020)
7. Glutamate → GABA
8. Lysine → Cadaverine (a diamine)
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Biochemistry

A. Glucokinase Q. Highest thermic effect is of which food? (INICET

B. Hexokinase May 2023)
C. PFK A. Carbohydrate
D. Glucose 6 phosphatase B. Fat
Exp: Glucose-6-phosphatase is an enzyme of C. Protein
gluconeogenesis, so a catabolic enzyme which is D. Mixed
activated by low insulin concentration and high
glucagon. Exp: Protein has the highest thermic effect of
food, meaning it requires more energy for digestion,
Q. RBC uses which of the following substances during absorption, and utilization compared to carbohydrates
fasting / starvation? (INICET July 2021) and fats.
A. Glucose
B. Ketones RATE LIMITING ENZYMES AND
C. Amino acids REGULATION
D. Fatty Acid
Glycolysis
Exp: RBCs rely predominantly on glucose as their
energy source, even during fasting or starvation, •• Three Regulatory /Irreversible Enzymes
as they lack mitochondria and cannot utilize other 1. Hexokinase /Glucokinase
substrates like ketones, amino acids, or fatty acids.
2. Phosphofructokinase-1 (PFK-1)
Q. Insulin inhibits which of the following lipase
3. Pyruvate Kinase
enzymes? (INICET July 2021)
A. Hormone sensitive lipase Gluconeogenesis
B. Lipoprotein lipase •• 3 Rate Limiting Enzymes
C. Acid lipase
1. Pyruvate carboxylase
D. Alkaline lipase
2. PEPCK (Phosphoenol Pyruvate carboxykinase)
Exp: Insulin is an anabolic hormone and inhibits
catabolic enzymes. HSL is a catabolic enzyme. 3. Fructose 1-6 Bisphosphatase (Most Important)

Q. In low insulin: glucagon ratio. What is correct? TCA Cycle / Kreb’s Cycle
(NEET PG 2023) •• 3 Rate Limiting Enzymes
A. Increase activity of HSL 1. Citrate synthase
B. Increase activity LPL
2. α-Ketoglutarate dehydrogenase
C. Increase glycogenesis
3. Isocitrate dehydrogenase: Most important
D. Increase glycolysis
ƒƒ Stimulated By ADP
Exp: HSL is a catabolic enzyme so activity increases
under low insulin (anabolic hormone) and high glucagon ƒƒ Inhibited by ATP and NADH
(catabolic hormone) concentration.

Q. Which of the following is found only in cytoplasm:

(FMGE Jan 2023)
A. TCA cycle
B. Beta-oxidation of Fatty acids
C. Glycolysis
D. Gluconeogenesis
Exp: All anabolic pathways occur in cytoplasm. Exception:
Glycolysis and Glycogenolysis (Catabolic pathways
occurring in Cytoplasm)
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Pathway Rate Limiting Enz Activators Inhibitors

Glycolysis PFK-1 AMP, fructose 2,6 bisphosphateQ ATP, Citrate
Glycogenesis Glycogen synthase Insulin, glucose 6-P Glucagon, Epinephrine
glycogen cAMP, kinase, S’AMP, Glucagon, Ca-calmodulin, Insulin, Phosphatase, ATP,
Glycogenolysis
phosphorylase Epinephrine, Nor – EpinephrineQ Glucose, Glucose-6-P, Fructose-1 P

Pathway Rate limiting Enz Activators Inhibitors

HMP G6PD NADP NADPH
PRPP Glutamyl
De novo purine synthesis - AMP, GMP, IMP
Amidotransferase
CPS-II (Euk) (carbamoyl
Pyrimidine synthesis ATP UTP
phosphate synthetase )Q
Urea cycle CPS - IQ NAG (N-Acetyl Glutanate) -
Purine Catabolism Xanthine oxidase - AllopurinolQ

Pathway Rate limiting Enz Activators Inhibitors

ketone body synthesis HMG Co-A synthase
Cholesterol body synthesis HMG CoA reductase Insulin, thyroxine Glucagon, cholesterol,
mevalonate, Bile acids, statins
Fatty acid synthesis Acetyl CoA carboxylase or Insulin, citrate Glucagon, Palnitoyl CoA / acyl
malonyl CoA synthetase CoA

Pathway Rate limiting Enz Activators Inhibitors

ß-oxidation of FA CPT – I or CAT – I (carnitine palmitoyl / acyl transferase) - Malonyl CoAQ

Bile acid synthesis 7-a-Hydroxylase - -

Catecholamines synthesis Tyrosine hydroxylase (requires Tetra Hydro Biopterin (THB), - -
NADPH)
Vitamin D synthesis 1-a-hydroxylase (in kidneys)

Pathway Rate limiting Enz Activators Inhibitors

Haem synthesis ALA Synthase - -
Niacin / Vit B3 synthesis QPR Tase (Quinolate Phospho Ribosyl Transferase) - -
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Biochemistry

Reciprocal Regulation:
2 opposite pathways never occur together:
1. Glycolysis & Gluconeogenesis: Fructose 2,6 Bisphosphate is the reciprocal regulator, which inhibits
gluconeogenesis and activates glycolysis, as it is formed in fed state.
2. Beta oxidation & Fatty acid synthesis: Malonyl CoA is formed in fed state in Fatty acid synthesis and it
inhibits CPT-1 (RLE of beta oxidation of Fatty acids)
G6PD deficiency Pyruvate kinase deficiency
Hemolysis Hemolysis
1st most common human enzyme deficiency 2nd most common human enzyme deficiency
Heinz bodies present Heinz bodies absent
•• In prokaryotes, RLE of Pyrimidine synthesis is: ATC (Aspartate Trans Carbamoylase)

ENERGETICS Total ATP generated during anaerobic conditions is =

In this chapter, energetics of following explained: 4ATP - 2 ATP = 2 ATP (No ATP’s from NADH produced
Glycolysis, RL Shunt, TCA cycle, Warburg effect, ETC, as seen in aerobic glycolysis)
NADH Shuttles, Urea cycle, Galactose & Fructose
Important Information
metabolism, Gluconeogenesis, Beta oxidation of Fatty
Acids & Ketone body breakdown. •• Purpose of extra step of lactate dehydrogenase
is to regenerate NAD which again can be used
Energetics Of Glycolysis in glycolysis to keep the glycolysis going.
Under aerobic conditions Q. In anaerobic glycolysis, End Product is?

A. 2 ATP + 2 NAD
B. 2 ATP
C. 2 ATP + 2 NAPH
D. ATP + 2 FADH2

Q. In Anaerobic glycolysis, there is gain of?

A. 2 ATP + 2 NAD
•• 2 ATP used: Hexokinase, Phosphofructokinase B. 2 ATP
•• 2 SLP give 4 ATPs as phase II of glycolysis C. 2ATP + 2 NADH
starts with 2 molecules of glyceraldehyde-3-
phosphate. D. 4 ATP + 2 FAPH2

•• Total ATPs generated = 7 ATPs (aerobic 2 ATP as net gain of NAD is ‘Zero’.
conditions).
Q. No. of ATP produced in RBCs in fed state, fasting
state, aerobic and anaerobic condition.
Under Anaerobic Condition
Ans. As there are no mitochondria in RBC, so, there
is no ETC. So, no ATP will be produced from NADH via
ETC. Hence, total ATP produced in RBC in fed, fasting,
aerobic or anaerobic state is always 4-2 = 2 ATP

Rapoport-Leubering Shunt / Cycle

•• Occurs only in RBCs
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Energetics of TCA Cycle

•• In RL Shunt, one substrate level phosphorylation

(SLP) step doesn’t occur (see fig).
•• Thus 2, 3-BisPG is produced at the expense of
2ATP. •• Dehydrogenases of TCA produce 3 NADH & 1
FADH2
•• Thus, ATP formed in RBC via RL shunt is 2 ATP
- 2 ATP = Zero ATPQ •• There is 1 SLP (Substrate level phosphorylation)
by succinate thiokinase
Important Information
•• So, from 1 acetyl CoA we get:
•• The purpose of RL shunt is not to produce
ATP but to form 2,3-BisPG –– 3 NADH → ET C → 7.5 ATP

•• 2,3-BisPG helps in release of O2 from HbA –– 1 FADH2 → ETC → 1.5 ATP

–– 1ATP/GTP → SLP → 1 ATP
Full Story of RBC
–– Total = 10 ATP per Acetyl CoA.

Energetics of complete breakdown of

Glucose

Important Information Pasteur’s Effect

•• If no RL Shunt occurs in RBCs, we get → 2 ATP •• Occurs in any normal cell
•• In phase II, •• In the presence of O2, Anaerobic glycolysis is
–– If one triose enters RL shunt we get → 1 ATP inhibited.

–– If two triose enters RL shunt we get → 0 ATP Warburg’s Effect

•• Occurs in cancer cells
•• In this, even in the presence of O2, glucose is
converted to lactate
•• Hence it is known as “Aerobic glycolysis”Q
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•• Lactate is the dead end of Glycolysis, so, no Important Information

oxidative phosphorylation further
•• Glycerol phosphate shuttle is more important
•• In conclusion, Warburg’s Effect is Aerobic
in brain and skeletal muscle as it provide quick
glycolysis with no oxidative phosphorylation
supply of energy.
•• But Here end-product is lactate and ATP
Q. Shuttle is used for?
formed = 2 ATPs
A. Glycolysis
ETC
B. TCA
•• NADH gives 2.5 ATP in ETC
C. Link Reaction
D. All
Ans: A) Because shuttles are required for transport
of NADH from cytoplasm to mitochondria whereas
TCA and link reaction already produce their NADH in
mitochondria. So, no shuttle is required by them.

Q. If aerobic glycolysis use glycerol-3-phosphate

•• FADH2 gives 1.5 ATP in ETC shuttle, how many ATPs are produced?

A. 2 ATP
B. 5 ATP
C. 7 ATP
D. 3 ATP
Ans. 5 ATP

•• Be careful what is asked: ATP from NADH/

FADH2 or from individual complexes I/II/
III/IV and answer accordingly.

Shuttles
•• NADH is starting material for ETC but it is
formed in cytoplasm whereas ETC occurs in
mitochondria.
•• 2 Shuttles help in transport of NADH across
the inner mitochondrial membrane (IMM) of
mitochondria.

Q
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Energetics of Urea Cycle Energetics of Galactose Metabolism

•• Here Glucose-6-P enters glycolysis directly

thus hexokinase is not used.
•• Therefore, energetics of Galactose metabolism
is same as glucose metabolism.
•• So, like glucose metabolism galactose
metabolism produces
–– under aerobic condition = 7 ATPQ
•• At CPS-I step- 2 ATP used –– under anaerobic conditions = 2 ATPQ
•• At arginosuccinate synthetase step: ATP is Energetics of Fructose Metabolism
converted to AMP which is equivalent to 2 ATP
consumed
•• So, total ATP used to make 1 urea = 3 ATP or 4
high energy phosphates

Important Information
•• CPS-I is absent in brain
•• Arginase is absent in kidneys, so last product
of urea cycle in kidney is arginine. So, source
of arginine (semi-essential) in body is kidneys.

•• Here 2 ATPs have been used to Form

Glyceraldehyde-3-P (GAP) which is equivalent to
phase I of glycolysis where too we use 2 ATPs.
•• Also, phase II of fructose metabolism is same
as that of glycolysis. Thus, fructose metabolism
energetics is same as glucose.
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Biochemistry

Important Information •• 2 Alanine → glucose via pyruvate → 6 High

energy phosphates
•• Fructose is the most rapidly metabolized
monosaccharide because Energetics of β-Oxidation of Fatty
–– It by-passes PFK-1 Step (rate limiting Acid
enzyme of glycolysis and a time-consuming
step)
–– So, Fructose rapidly forms Pyruvate →
Acetyl CoA → Fats. That’s why Fructose
Is also the Most Lipogenic Sugar

Gluconeogenesis Energetics Activated FA from cytoplasm reaches mitochondria

through carnitine systemQ

•• CPT-I (Carnitine Palmitoyl Transferase -I) is

Energetics the rate limiting enzyme.
•• 2 ATP used by Pyruvate carboxylase –– In fasting state, it allows acyl-CoA to go into
•• 2 GTP used by PEP carboxykinase mitochondria

•• 2 ATP used by Phosphoglycerate Kinase –– In fed state, it does not allow acyl CoA to go
into mitochondria
•• So, 4 ATPs and 2 GTPs or 6 high energy
phosphates are used to make 1 glucose from 2 •• Liver – Mitochondria
pyruvate –– Here activated FA comes for β-oxidation
•• Lactate gets converted to pyruvate and most commonly from Palmitic Acid(16C)
pyruvate is used in gluconeogenesis; no ATP is
used or produced from lactate to pyruvate.
•• Alanine is the most glucogenic amino acidQ
which is converted to glucose; Alanine gets
converted to pyruvate by Alanine transaminase
(here also no ATP used or produced)

ATP used for various substrates

•• 2 pyruvates → glucose → 6 High energy
phosphates
•• 2 lactates → glucose via pyruvate → 6 High
energy phosphates
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–– 4 ATP produced via SLP

–– 2 ATP used each by (Hexokinase, PFK-1)
•• End products of liver glycogen is glucose, thus
ATP formed here = 2
•• But, end-product of muscle glycogen is glucose-
6-P. Thus, when it enters glycolysis, hexokinase
is not required and there is one less use of ATP.
•• Therefore, Net ATP synthesis = 4 SLP ATP -
1 ATP consumed by PFK-1 = 3 ATP

Energetics of Ketone Body Breakdown

Energetics from acetoacetate
Fate of acetyl CoA
•• Acetoacetate gets converted into 2 molecules
•• 1st → TCA of acetyl CoA
•• 2nd → KB synthesis •• 2 Acetyl CoA =20 ATP
•• 3rd → Activation of 1st step of Gluconeogenesis •• 1 less because Succinyl CoA → Succinate does
•• When acetyl CoA goes into 2nd or 3rd fates, not yield any ATP
we don’t get 80 ATPs which are generated if it •• Acetoacetate = 19 ATP
goes under TCA.
Energy From β-OH Butyrate
Q. In β-oxidation of Palmitic acid if final product is
acetoacetate then net gain of ATP is?

A. 21
B. 26
•• 1 NADH = 2.5 ATP
C. 106
•• So, for β-hydroxy butyrate total ATP produced
D. 12.9
will be = 19 (from acetoacetate) + 2.5 (from 1
Ans. B NADH) = 21.5
•• As it will not be used in TCA cycle. So, 80 ATP
Important Information
will not form.
Pathways producing zero ATPQ
•• Instead acetoacetate will form ketone bodies.
•• HMP
•• Hence, only 28 ATP are produced
•• Uronic acid pathway
•• So, net gain = 28-2 (2 ATP required for
activation of FA = 26 ATPs •• RL shunt

Q. If muscle glycogen is used for anaerobic glycolysis, •• Oxidation of VLCFA

how many ATPs are formed? •• α-oxidation of FA
A. 2
B. 7
C. 3
D. Zero
Ans. C.
•• Normally in anaerobic glycolysis
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Biochemistry

Lysosomal Storage Diseases •• This enzyme lies in Golgi apparatus and make
•• If some lysosomal enzyme (Hydrolases) is/ hydrolases reach to lysosomes.
are absent or deficient, then that particular •• If this enzyme is defective, hydrolases will not
substrate (mostly macro-molecule) accumulates reach lysosome.
and get stored in lysosomes giving rise to
lysosomal storage disorders. •• It is also known as protein targeting disorder
as protein do not reach its target organelle
1. Mucopolysaccharidosis (MPS)
•• Clinical features
2. l-cell disease
–– Same as MPS
3. Pompe’s disease (also a Glycogen Storage
Disease) –– Serum hydrolase ↑↑

4. Sphingolipidoses 3. Pompe’s Disease

5. Wolman’s disease •• Glycogen storage disease
6. Cystinosis •• Enzyme deficiency: Acid maltaseQ

1. Mucopolysaccharidosis (MPS) •• Usually occur in children and child dies within 2

years of age
Hurler’s Disease Hunter’s disease
•• Clinical features: Hypotonia, Hepatomegaly &
Enzyme deficient: α-L- Enzyme deficient: Iduronate CardiomegalyQ
Iduronidase Sulfatase
Corneal clouding Corneal clouding absent 4. Cystinosis
present (Clear vision)Q •• Defect in cystine transporter
•• Cystine get deposited in lysosomes in various
parts of body
•• Rx: take cysteamine, which chelates cystine
•• Here, cyanide nitroprusside test is positive.

5. Sphingolipidoses
•• Dermatan sulfate •• Dermatan sulfate
+ Heparan Sulfate + Heparan sulfate
accumulation accumulation
•• AR •• XR (So, mostly males
patients)Q
•• Severe and Inguinal •• Known as Mild Hurler with
Hernia present aggressive behaviour
•• Reilly Bodies •• Reilly Bodies Inclusions
Inclusions found not found mostly

2. I Cell/Inclusion body Disease

•• Enzyme deficiency: N-acetyl glucosamine
phosphotransferaseQ
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Important Information
•• Fabry’s disease: Only sphingolipidosis which is
X-linked recessive as all others are autosomal
recessive.
•• No Mental Retardation in Gaucher’s disease
(as glucocerebroside is not found in CNS)Q
•• No hepatosplenomegaly in Tay Sach’s disease
as gangliosides are absent in liver
•• All Sphingolipidoses have cherry red spot Clinical feature of Fabry’s disease:
except Fabry’s, Gaucher’s & Krabbe’s disease
Angiokeratomas: Benign cutaneous lesion of capillaries,
•• Sphingolipidoses with angiokeratoma: Fabry’s resulting in small marks of red to blue color &
disease- this also resembles Sickle cell crisis characterized by hyperkeratosis.
•• SLP resembling Rheumatoid arthritis: Farber’s
DiseaseQ
6. Wolman’s Disease
•• Enzyme deficient: Acid lipaseQ
Clinical images related to Sphingolipidoses:
•• It is lysosomal storage disease but not a
sphingolipidosis.
•• It is also k/a cholesterol ester storage disease
as here TG & cholesterol esters accumulate.
•• Pathognomonic feature is calcification of
adrenal glandsQ
•• Other clinical features
–– Watery green diarrhoea
–– Relentless Vomiting and failure to thrive
–– Hepatosplenomegaly

Crumpled paper appearance of macrophages called

Gaucher’s cell in Gaucher’s disease

Calcification of adrenals

Protein Targeting Disorders

Disorder is in targeting/sending the protein
at a particular site

Macular cherry red spot 1. I-Cell disease

2. Primary hyperoxaluria
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Biochemistry

3. Zellweger Syndrome
•• Most severe peroxisomal biogenesis disorder
•• Organelle affected is peroxisomes, so that no
enzymes reach there (‘ghost’ peroxisomes)
•• In peroxisomes, α-oxidation occurs, which
breaks down Phytanic Acid. And oxidation of
VLCFA (Very Long Chain Fatty Acids)Q
•• In this disease, both these processes do not
occur, causing accumulation of phytanic acid &
VLCFA.
4. Cystic fibrosis
5. Familial Hypercholesterolemia

Clinical features of Zellweger syndrome Type I - Von Gierke’s Disease: most common GSD in
children- Clinical features
•• Severe hypoglycemia
•• Massive hepatomegaly & kidneys also enlarged
due to glycogen accumulation
•• Ketosis
•• Hyperlipidemia
•• Moon like/round/Doll like faces
•• Lactic acidosis
•• Hyperuricemia
High Forehead
Clinical features of Von Gierke’s disease
Garrod’s Tetrad
•• Inborn errors of metabolism
•• 4 diseases MNEMONIC: CAAP
–– C - Cystinuria
–– A - Alkaptonuria
–– A - Albinism
–– P - Pentosuria (Essential Pentosuria) - enzyme
deficient is Xylulose Reductase or Xylitol
Dehydrogenase

Glycogen Storage Diseases

Hepatosplenomegaly
•• If Liver affected → C/F - Hypoglycemia
•• If Muscle affected → C/F - Exercise intolerance
& muscle cramps
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AMINO ACID TRANSPORTER DEFECTS - Common

feature is that amino acid not increased in blood, but
getting excreted in urine

Defect in
Disorder Amino acid in urine
transporter
CystinuriaQ MNEMONIC: COAL
(m/c Transporter for C - Cystine
transporter basic amino acid & O - Ornithine
defect) Cysteine A - Arginine
L - Lysine
Common
transporter for
Doll like facies
Hartnup’s tryptophan and Tryptophan (mainly)
Organ Affected in Type II, III and IV are: Muscles, DiseaseQ neutral amino acids and Neutral amino
Liver and Brain (mono-amino-mono- acids
Important Information carboxy amino acid
transporter)
•• If a GSD Q given with Muscle, Liver and Brain
Common
affected, then its easy to solve: Glycinuria
transporter for Glycine & Proline
•• Its clear that it can be either Type II, III glycine & proline
or IV
–– If Lysosomes mentioned in the Q then it Important Information
is Type II
•• In Hartnup’s disease
–– If you see limit dextrins in the Q then it is
–– Patient have pellagra i.e. Vit-B3 deficiency
Type III & if amylopectins given in the Q,
as tryptophan has role in forming Vit-B3
then type IV
(60 mg Tryptophan makes 1 mg Niacin)
Type V - Mc Ardle’s disease
–– Serum tryptophan levels not raised
•• Most common GSD in Adults
•• Characteristic feature: Lactate normal (not
Amino Acid Disorders
increased) after exerciseQ Glycine disorders
Important Information Non-ketotic
Hyperoxaluria Glycinuria
•• In Type 1 - Blood glucose level does not increase hyperglycinemia
after glucagon hormone •• Glycine •• Glycine •• Glycine cleavage
•• In Type III - Blood glucose level increase after transaminase transporter system defect
glucagon in fed state but not in fasting state deficient/ defect •• C/f
•• Cori’s disease - Glycogen accumulated with short defective •• C/f ○○ ↑ glycine in
outer branches •• C/f ○○ ↑ glycine serum, urine
•• Anderson’s disease - Glycogen accumulated with very
○○ ↑ oxalate in urine and CSF
long outer branches
in urine ○○ Urine ○○ Mental
•• Normal structure glycogen accumulated in Von
Gierke’s and Her’s disease ○○ extra oxalate retardation
•• Recombinant enzyme → recombinant human GAA renal normal ○○ Seizures
→ rhGAA; alglucosidase alpha, Myozyme → used in oxalate ○○ Risk of
Pompe’s disease deposits oxalate
•• GSD Type VII (Tarui disease) → deficiency of PFK-1 ○○ Oxalate stones
•• GSD Type 11 (XI) → Fanconi Bickel syndrome → stones
GLUT-2 mutation Q
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Biochemistry

Phenylketonuria (PKU) Maple Syrup Urine Disease (MSUD)

•• Enzyme deficient: Phenylalanine hydroxylaseQ •• Enzyme deficient: Branched Chain Keto Acid
(BCKA) dehydrogenase or decarboxylaseQ
•• Accumulation of Branched chain amino acids and
keto acids occurs
•• Urine odor is of Burnt sugar / Maple syrup
odor
•• Clinical features
[Phenyl-keto-uria → phenyl- keto acid (phenyl Pyruvate) –– Mental Retardation
- in urine] –– Ketosis
•• C/F
–– If untreated, coma & death can occur
–– Mousy/musty body odour (due to
phenylacetate)Q –– Has high mortality rate
–– Severe MR (due to Phenylalanine) •• Rx
•• Diagnosis 1. Vitamin B1 supplementation (coenzyme for
–– FeCl3 urine test → Green colour (d/t Phenyl BCKA dehydrogenase)
Pyruvate)Q 2. Dietary restriction of Branched Chain Amino
•• Rx Acids

1. Lifelong Restriction of phenyl alanine in diet Alkaptonuria/Black bone disease

ƒƒ Aspartame (artificial sweetener) is contraindicated •• Enzyme defect: Homogentisate dioxygenase
as aspartame is made of Aspartate + Phenylalanine (previously k/a Homogentisate oxidase)Q
2. Give Tyrosine & Tryptophan •• Homogentisic acid accumulates
3. Tetra Hydro Biopterin (THB) Supplementation •• C/F
helps in some patients
–– On standing color of urine turns black due to
Clinical Features of phenylketonuria oxidation of Homogentisic acid
–– Age of onset: 30 - 40 years
–– no MR (Mental Retardation)
–– Homogentisic acid gets polymerized in to
alkapton bodies which accumulates in:
→ Cartilages (Nose, Ear Pinna, IV discs):
Arthritis
→ Connective tissue: Bluish black colour
→ Intervertebral discs: lower back pain
(due to
–– Collectively, accumulation of homogentisic
acid in all body parts is termed as Ochronosis
and arthritis as Ochronotic arthritis.

Clinical features of AlkaptonuriaQ

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1. Acquired
•• Due to vitamin B6, B9 and B12 deficiency
2. Genetic
•• Due to Enzyme Cystathionine beta Synthase
defectQ
•• Here cysteine becomes essential.
•• c/f
–– ↑ Serum Homocysteine (has SH - group)
–– ↑ urine Homocystine (made of two
homocysteine joined by S-S bond)
Cyanide nitroprusside test is positive.

Clinical features of homocystinuria

Albinism
•• Enzyme deficient: Tyrosinase (makes melanin
from tyrosine)
•• Tyrosine is an oxidase enzyme & requires copper
for its action.
•• c/f
•• Hypopigmentation (milky white skin, Blonde Important Information
hair, and Red eye color)
•• How to distinguish between vit B6, B9 and B12
deficiency
Vitamin
Substrate accumulated
deficiency
B6 Homocysteine, Xanthurenic acid
Homocysteine, FIGLU (Form Imino
B9
GLUtamate)
B12 Homocysteine, L-methyl malonyl acid
Important Information
Vitiligo
•• Patchy hypopigmentation
•• Tyrosinase is normal

Homocystinuria (HCU)
Two types:
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Biochemistry

DISORDERS OF CARBOHYDRATE •• Accumulation of Fructose-1-P occurs in liver &

kidney.
METABOLISM
•• Clinical features
Galactosemia
Minor Classical (M/C Galactosemia) –– Jaundice and hepatomegaly
–– Hypoglycemia (as fructose-1-PO4 inhibits
•• Enzyme deficient: •• Enzyme deficient: GALT liver glycogen phosphorylase thereby
Galactokinase [Galactose-1- PO4 uridyl blocking glycogenolysis)
•• C/F transferase]Q
–– If untreated it causes renal failure
○○ Oil drop •• GALT converts Gal-1-P to
cataract UDP-galactose Features Disease
•• Accumulation of galactose-1 CNS, Skin and hair affected Multiple carboxylase
-PO4 with Tom cat urine odor deficiency
•• C/f
CNS affected +
○○ Oil drop cataract PKU
hypopigmentation
○○ Jaundice & Hepatomegaly
CNS affected + Burnt sugar
○○ Mental retardation MSUD
odour

Child (young person)

Clinical features of galactosemia with stroke, skeletal
abnormalities, knock knees, HCU
pectus carinatum, elongated
limbs

Patient with organomegaly,

easy bruising, bony pain and Gaucher’s disease
frequent fractures

Coarse facial features Lysosomal storage disease

Snow-flake cataract Diabetes

Oil drop cataract Galactosemia

Sunflower cataract with KF Wilson’s disease due to

ring Cu def

Oil drop cataract

Hereditary Fructose Intolerance

•• Enzyme deficient: Aldolase B
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PREVIOUS YEAR QUESTIONS C. Alkaptonuria

D. MSUD
Q. Glutamine is increased in CSF, blood & urine in
which defect? (NEET Jan 2019) Exp: Alkaptonuria is a metabolic disorder
characterized by a deficiency of homogentisic acid
A. Arginosuccinate Synthetase oxidase, leading to the accumulation of homogentisic
B. OTC acid, which causes dark urine and pigmentation of
C. CPS – I various tissues.
D. Arginase Q. What is seen in G6PD deficiency ? (INICET July
Exp: In all given enzyme deficiency, ammonia will 2021)
increase but CPS-1 is rate limiting enzyme, so it will A. Decrease membrane lipid peroxidation
increase ammonia most & increase in ammonia lead to
B. Decrease generation of reduced glutathione
increase in glutamine.
C. Decrease NADH generation
Q. A boy develops hypoglycemia after moderate D. Decrease scavanging of RBC by macrophages
activity. Blood report shows raised ketones, lactic acid
E. Hemolysis
and triglycerides. On examination, liver and kidney
were found to be enlarged and patient is diagnosed Exp: Glucose-6-phosphate dehydrogenase (G6PD)
with Von Gierke’s disease. Which enzyme deficiency deficiency leads to hemolysis of red blood cells,
he has? (FMGE Dec 2020) particularly under conditions of oxidative stress due
to low availability of NADPH and reduced form of
A. Glucose 6 phosphatase
Glutathione.
B. Acid Maltase
C. Glycogen synthase Q. In MSUD (Maple Syrup Urine disorder) which of
the following is not restricted: (INICET May 2022)
D. G-6-PD
A. Methionine
Exp: Von Gierke’s disease: enzyme deficient is Glucose
6 phosphatase, leading to impaired glucose release B. Valine
from glycogen and resulting in hypoglycemia and other C. Leucine
metabolic abnormalities D. Isoleucine

Q. Glycogen stored in liver in all the following Exp: In MSUD, the branched-chain amino acids
conditions except? (FMGE Aug 2020) (leucine, isoleucine, and valine) are restricted in the
diet, due to defect in their catabolism.
A. Gaucher’s disease
B. Cori’s disease Q. Brunt sugar smell of urine is due to the defect of?
C. Mc Ardle’s disease (INICET Nov 2022)
D. Pompe’s disease A. Phenylalanine hydroxylase
Exp: Gaucher’s disease, is a lysosomal storage disorder B. Isovaleryl CoA dehydrogenase
of sphingolipids and not glycogen, but all others Cori’s C. Fumarylacetoacetate hydrolase
disease, Mc Ardle’s disease, or Pompe’s disease are D. Branched chain keto acid dehydrogenase
Glycogen storage disorders.
Exp: Burnt sugar like odor is a characteristic feature
Q. A 40-year-Old Male Patient come in OPD and of Maple Syrup Urine Disease (MSUD) which occurs
complaining of long-standing black Urine ferric due to the inherited deficiency of branched Chain
Chloride and Benedict’s test both were found to be Keto-acid dehydrogenase.
positive in this patient. Pinna and sclera of eyes have
Q. Zellweger syndrome is caused by the defect of
black pigmentation. What is your diagnosis? (FMGE
which of the following organelles? (INICET Nov 2022)
Dec 2020)
A. Mitochondria
A. Phenylketonuria
B. Lysosomes
B. Galactosemia
C. Peroxisomes
D. Nucleus
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Biochemistry

Exp: In Zellweger syndrome, there are empty C. Tarui’s disease

peroxisomes in all body cells causing defect in alpha- D. Anderson’s disease
oxidation and oxidation of VLCFA. It is the most
severe Peroxisomal Biogenesis Disorder (PBD). Exp: Mc Ardle’s disease is characterized by deficient
glycogen phosphorylase in muscle cells, leading
Q. A young male with a H/o dyslipidemia having ABC-A1 to impaired glycogen breakdown and decreased
mutation shows the following. See the image and tell availability of glucose for energy production during
the diagnosis. (INICET Nov 2022) exercise.

Q. A 4-year-old child easy fatigability. The mother

also complained that the child was more hungry
between meals, and the child recovers after food.
Liver examination revealed no glycogen? (NEET PG
2023)
A. Branching enzyme
B. Debranching enzyme
C. Glucose 6 phosphatase
D. Glycogen synthase
A. Wolman’s Disease
B. Gaucher’s Disease Exp: Glycogen synthase deficiency (also known as
Glycogen Storage Disease Type 0) leads to impaired
C. Tangier’s disease
glycogen synthesis in the liver, resulting in low glycogen
D. Tay Sach’s disease stores and symptoms such as fatigue and hunger
Exp: Large orange/ yellow tonsils (due to fat Q. A child presented with difficulty in vision on
deposition) are a characteristic feature of Tangier’s examination cherry red spots were seen on macula.
disease due to defect in ABC-A1 transporters. There was no organomegaly. Identify the disease.
Q. Identify the given image (INICET Nov 2022) (NEET PG 2023)
A. Gaucher disease
B. Hunter disease
C. Tay-Sachs disease
D. Niemann pick disease
Exp: Tay-Sachs disease is characterized by a
deficiency of the enzyme Hexosaminidase A, leading
to the accumulation of gangliosides in the brain and
retina, causing vision problems and cherry red spots
on the macula.

Q. In Pompe’s disease, enzyme deficiency is? (INICET

A. Gaucher’s disease May 2023)
B. Wolman’s disease
A. Lysosomal acid alpha glucosidase
C. Niemann pick disease
B. Phosphofructokinase
D. Fish eye disease
C. Muscle glycogen phosphorylase
Exp: The given image shows crumpled tissue D. Lactate dehydrogenase
paper appearance of macrophage cells which is a
characteristic feature of Gaucher’s disease Exp: In Pompe’s disease, there is a deficiency of the
enzyme lysosomal acid alpha glucosidase (also known
Q. A child was fatigued after exercise and the blood as acid maltase), which leads to the accumulation of
sample collected soon after exercise showed low glycogen in lysosomes and subsequent muscle and
glucose and lactate level. The probable diagnosis is. organ dysfunction.
(NEET PG 2023)
Q. Xanthurenic Acid in urine indicates: (INICET May
A. Mc Ardles disease 2023)
B. Von Gierke’s disease
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A. Vitamin B6 deficiency Optical Isomerism

B. Vitamin B1 deficiency
•• When plane polarized light is allowed to pass
C. Niacin deficiency through the solution of carbohydrate, then it
D. Vitamin B2 deficiency gets rotated:
Exp: Xanthurenic acid in urine is an indicator of niacin –– If it gets rotated to right side, the compound
(vitamin B3) deficiency. It is formed when tryptophan is called dextro-rotatory and designated as
metabolism is impaired due to insufficient niacin levels. d or (+) isomer
–– If it gets rotated to left side, the compound
CARBOHYDRATE CHEMISTRY
is called levo-rotatory and designated as l or
Carbohydrates (-)

Definition: Poly hydroxy (many OH) Aldehyde or Structural isomerism

Ketones
•• 4 Types
•• Number of OH groups are always one less than
1. Functional Isomers → Different functional group
the number of carbons. e.g. Glucose (6C) has 5
(aldehyde or keto)Q
OH & Ribose (5 C) has 4 OH groups

Isomerism
•• Isomerism is possible due to Asymmetric/chiral
carbon
–– Asymmetric C - When all of 4 valencies of
C are occupied by different atoms/group of
atoms. e.g.

•• Both carbohydrates and amino acids have

Asymmetric C, so both show isomerism.
Important Information:
–– C2 to C5 are asymmetric carbons in glucose,
•• Racemic mixture (equal d & l) So, it is optically so total 4 asymmetric carbons
inactive
2. Enantiomers- D-L isomerism/Mirror imagesQ
•• Racemase enzyme: Enzyme which interconverts
•• Different H & OH orientation around the 2nd
‘D’ ↔ ‘L’ not d and l. Thus, name Racemase is a
last carbon
misnomer. D & L are structural isomers, but d
& l are optical isomers.

Isomerism is of 2 Types:
1. Structural isomerism a.k.a. stereoisomerism (same
molecular formula, different Structure)
2. Optical isomerism (same molecular formula,
different optical properties)
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Biochemistry

4. Anomerism

•• Seen only in cyclic structures

•• Anomers have different H and OH orientation
around functional carbon (C1 or C2)

Important Information
•• In case of carbohydrates → D-Form is
abundant.
•• In case of amino acids in Proteins → L-form Important Information
is abundant.
•• Pyranose: Six membered ring with 5 C & 1 Oxygen
•• Free amino acid (Amino acid not in protein) → •• Furanose: Five membered ring with 4 C & 1 Oxygen
can be L or D Form, e.g. D-serine & D-aspartate ○○ Glucose → mainly Pyranose
(Found in brain)
○○ Fructose → mainly Furanose
•• Amino acid synthesized in body → L-form ○○ Hexoses (6C) → Both Pyranose & Furanose exists
•• Source of D-Amino acid → always exogenous ○○ Pentoses (5C) → Only Furanose exists
(Diet or Bacteria flora)
Anomers are of two types- alpha and beta

Q. Which form of amino acid is present in body?

Ans: Both D & L

Q. Which form of amino acid is present in proteins?

Ans: Only L

3. Epimerism

•• Different H or OH orientation only around one

Glucose Transport
carbon other than penultimate Carbon •• Methods
–– Mannose is epimer of glucose at C2 Active (Secondary) Facilitative Diffusion
Transport
–– Galactose is epimer of glucose at C4
•• Na-dependent Glucose •• Na-independent GLUTs
•• But mannose and galactose are not epimers of Transport (SGLT) (GLUcose Transporters)
each other •• Occurs against •• Occurs down the
concentration concentration gradient
gradient
•• Bidirectional (allow both
•• Unidirectional (only
entry as well as exit of
allow entry of glucose
into the cell)Q glucose from cell)Q
•• Also called Na-Glu
symport
•• ATP is indirectly
used for Na+/K+
ATPase pump. So, it
is a secondary active
transport.
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Types of SGLTs 3. Dextran → used as plasma volume expander

Transporter Sugar transported Location 4. Cellulose → made of β-glucose
Name
5. Inulin → made of β-fructose
SGLT-1 Glucose and Galactose Both Intestine
and kidneys 6. Chitin → made of N-acetyl glucosamine
SGLT-2 Glucose only Only Kidneys Hetero-Polysaccharides: made of repeating unit of
Amino sugar & Uronic acid (oxidation at C6)
•• Mutation in SGLT-1 leads to Glu-Gal
malabsorption •• Only GAG which is not
sulfatedQ
•• Mutation in SGLT-2 leads to Familial Renal
•• Longest GAG
glycosuria or Renal Glucosuria
Hyaluronic Acid •• Has role in wound healing
and cell migrationQ
•• Located in Synovial Fluid &
Vitreous humour
•• Most abundant GAGQ
Chondroitin Sulfate
•• Present in Cartilage, Bone,
(CS)
Tendon
•• Found in Skin, Blood
Dermatan Sulfate (DS)
vessels, heart valves
•• Only GAG without uronic
acidQ
•• Most heterogenous GAG
Keratan Sulfate
•• Present in cornea &
connective tissue
Types of GLUTs
•• Responsible for
Name Tissue Location Function
Transparency of corneaQ
Brain, RBC, Placenta,
GLUT-1 Basal Glucose Uptake •• More sulphated than
Kidneys
Heparan sulfate
Intestine- absorption
•• Highest negative charge
Liver- Glycogen
Liver, Pancreas, •• Very good but costly
GLUT-2 formation
Intestine, Kidneys anti-coagulant (prevent
Pancreas- Insulin
coagulation but do not
secretion Heparin
dissolve clots)
Brain (Neuronal),
GLUT-3 Basal Glucose uptake •• Activates antithrombin III
Placenta, Kidneys
to slow down or delay the
Skeletal muscles, Insulin stimulatedQ progression of DVT
GLUT-4 Cardiac muscles, Glucose uptake after •• Released from mast cell &
Adipose tissues meals liver
Small intestine, •• Present on cell surfaces
GLUT-5 Testis (Sperms), Fructose transport Heparan Sulfate (HS) •• Has a role in cell–cell
Kidneys
adhesion e.g. retinal cell-
cell attachment.Q
Polysaccharides
Homopolysaccharides – made of same carbohydrate
units
1. Starch → made of α-glucose (storage form in plants)
2. Glycogen → made of α-glucose (storage form in animals)
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Biochemistry

Proteoglycan Glycoprotein

Carbohydrate >> Protein Protein >> Carbohydrate

Carbohydrate is either a mono-

Carbohydrate is always
saccharide or, oligosaccharide
a Heteropolysaccharide
but never a Polysaccharide
e.g. Aggrecan is a
e.g. Fibrous protein- Collagen,
proteoglycan made of 2. Benedict’s testQ
All plasma proteins except
Chondroitin sulfate and
Albumin •• Given positive by reducing sugars
protein
•• a semi-quantitative test as different colors
Fibres gives an idea of the amount of sugar present

Insoluble fibres Soluble fibres

•• Excreted unchanged •• Absorbs H2O & converted
from intestine to Gel form, which is
•• Examples: excreted
1. Cellulose •• Better in preventing
2. Hemicellulose Constipation
•• Provide more osmotic load
to intestine
•• Examples:
1. Pectins
2. Gums
3. Inulin Test For Ketone Bodies

Disaccharides Rothera’s TestQ

Glycosidic •• Done for detection of ketone bodies
Disaccharides Constituents Nature
bond
•• A positive Rothera’s test is when purple color
Maltose Glucose + Glucose α (1→4) Reducing ring is seen at the junction of two liquids
Isomaltose Glucose + Glucose α (1→6) Reducing
Non-
Trehalose Glucose + Glucose α (1→1)
Reducing
Glucose + Non-
Sucrose α (1→2)
Fructose Reducing
Galactose +
Lactose β (1→4) Reducing
Glucose
Tests For Amino Acids And Proteins
Tests For Carbohydrates
Ninhydrin Test
1. Molisch test
•• Done for detection of α-amino acids
•• General test given by all carbohydrates
•• Positive Ninhydrin test = Purple colour solution
•• Condition: No. of carbons must be ≥ 5
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Biuret test A. Liver

B. Pancreas
•• It is done for detection of proteins and peptides
C. Muscle and adipose tissues
•• Positive Biuret Test = purple colour solution
D. Placenta
•• A tripeptide and higher peptides will give a
Exp: Insulin facilitates glucose uptake by muscle and
positive test.
adipose tissues by promoting the translocation of
glucose transporters (GLUT4) to the cell membrane.

Q. A 15-year old boy, a known case of type I DM,

undergoes the following test for the detection of KB.
Which is this test: (INICET May 2023)

OSAZONES: are crystals formed by Reducing sugars,

can be seen in microscope

A. Rothera’s Test
B. Benedict’s test
C. Seliwanoff’s Test
D. Biuret Test
Exp: The Rothera’s test is used to detect the presence
of ketone bodies (ketones) in the urine, which can be
elevated in conditions like diabetic ketoacidosis.

CARBOHYDRATE METABOLISM
GLYCOLYSIS or EMP (Embden Meyerhof pathway)
•• Inhibitors of Glycolysis
•• Iodoacetate & Arsenite → inhibits glyceraldehyde-
3-P dehydrogenase
PREVIOUS YEAR QUESTIONS –– Na Fluoride → inhibits Enolase (used in blood
glucose estimation)
Q. A patient report is as follows; FPS - 82: PPBS -
140; Urine was found to be positive for benedict test. Important Information
What is the probable diagnosis? (JIPMER - Dec -
•• When arsenite inhibits glycolysis, then no
2019)
ATP is produced but glycolysis continues, and
A. Renal glycosuria pyruvate is formed.
B. Transient glycosuria
C. Alimentary glucosuria Irreversible steps / Substrate level
D. DM Regulatory steps phosphorylation (SLP)
1. Hexokinase 1. PG Kinase
Exp: The presence of glucose in the urine (positive
Benedict’s test) in a patient with normal fasting 2. PFK 1 2. Pyruvate Kinase
and postprandial blood sugar levels suggests renal 3. Pyruvate Kinase
glycosuria, which is a benign condition.
Link Reaction
Q. Which of the following tissues are dependent on
Enzyme - PDH (Pyruvate Dehydrogenase) complex,
insulin for glucose uptake (INICET Nov 2022)
irreversible reaction, occurs in mitochondria
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Biochemistry

Important Information
Malate (4C): Intermediate of TCA Cycle
Malonate (3C): Inhibitor of TCA Cycle
Malonate / Malonyl CoA is an inhibitor of:
1. TCA Cycle (inhibits Succinate Dehydrogenase)
2. ETC (inhibits Complex II)
3. Beta Oxidation of Fatty Acids (inhibits CPT-1)

Important information
•• 5 coenzymes are required for release of
energy from link reaction & TCA: Lipoic acid,
B1, B2, B3, B5. So, multivitamins are given
•• In B1 deficiency (Beri-Beri) or PDH complex during LethargyQ
deficiency, lactic acidosis will occur due to
excess pyruvate converting in to lactate in ETC
cytoplasm. •• Components of ETC (Located in Inner
Mitochondrial Membrane)
TCA Cycle
–– 5 protein complexes (I to V)- fixed within
•• Vital cycle of cell (occur in fed as well as fasting
the membrane
state), occurs in mitochondria in aerobic state
–– 2 Mobile molecules: Coenzyme Q and
•• TCA depends on 2 things:
Cytochrome C (a Peripheral membrane protein)
–– Energy status of cell: If ATP present, TCA
Note: Coenzyme Q is the only non-protein component
will not occur & vice-versa.
of ETC
–– Availability of oxaloacetate: Oxaloacetate
–– In ETC, oxidation & phosphorylation occur
is also regarded as carrier of TCA cycle or
together (coupled).
1st Substrate of TCA cycle. Also, it plays a
catalytic role in TCA cycle. –– Uncoupling means that oxidation occurs but
not phosphorylation.
Important Information
•• Uncouplers e.g.
•• Only 1 SLP occurs in TCA done by enzyme succinate
thiokinase which mostly produces ATP, but in liver & –– Dinitrophenol (drug)
kidney during fasting/starvation state, it produces –– Natural/Physiological uncouplers
GTP, as during this state, gluconeogenesis occurs & it
1. Thermogenin: present in brown fat in
requires GTP.
hibernating animals & in neonates & is
•• Acetyl CoA is not an intermediate of TCA cycle. responsible for non-shivering thermogenesis
•• 2 CO2 which are removed in TCA comes from
2. Thyroxine
Oxaloacetate. If oxaloacetate not given, then mark
Acetyl CoA. 3. Free fatty acids

Inhibitors of TCA Important Information

•• Malonate (3C) → Inhibits Succinate dehydrogenaseQ Q. ADP to ATP conversion in ETC is inhibited by?
•• Arsenite → Inhibits α-ketoglutarate Ans. Oligomycin (inhibits complex V which converts ADP
dehydrogenaseQ to ATP)
•• Fluorocitrate → Competitively inhibits Aconitase Q. ADP to ATP transfer in ETC is inhibited by?
•• Fluoroacetate → Non- competitively Inhibits Ans. Atractyloside (inhibits ADP-ATP translocase, which
Aconitase transfers ADP & ATP)
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Inhibitors of ETC ComplexesQ

Complex Inhibitor
Complex I Rotenone, Phenobarbitone, Amobarbital,
Piericidin A
Complex II Malonate (3C)
Carboxin (fungicide)
TTFA (Thenoyltrifluoroacetone)
Complex III Phenformin, Antimycin A
BAL {British anti-Lewisite} or
Dimercaprol
Important Information:
Complex IV CO, CN, H2S, Sodium Azide •• If both leucine and lysine are given in options for
ketogenic amino acid, mark leucine as it is more
Gluconeogenesis ketogenic

•• 4 Enzymes of Gluconeogenesis which are •• Purely ketogenic amino acids = 2

different from Glycolysis (refer fig in •• Purely glucogenic = 13
Energetics) •• Total ketogenic = 2+5 = 7

Enzyme Feature •• Total Glucogenic = 13+5 = 18

•• Present in mitochondria
Pyruvate carboxylase Reciprocal regulation of Glycolysis &
•• Uses ATP
•• Activated by acetyl CoA Gluconeogenesis
PEPCK
(Phosphoenolpyruvate
Both are present is cytoplasm
carboxykinase)
Fructose -1-6-
Bisphosphatase
•• Present in endoplasmic
reticulum (to prevent glucose-
6-P breakdown to glucose in
cytoplasm)
Important Information
•• Common enzyme of
Glucose-6 - •• Fructose 1,6-Bisphosphate compound → Glycolysis
gluconeogenesis and
phosphatase intermediate
Glycogenolysis
•• Present in liver but absent in •• Fructose 1,6-Bis Phosphatase enzyme →
muscles Gluconeogenesis enzyme

•• Deficient in Von Gierke’s •• Fructose 2,6-Bisphosphate compound → Reciprocal

disease Regulator
•• Fructose 2,6-Bis Phosphatase enzyme → active in
•• Substrates of Gluconeogenesis
Cancerous cells (not in normal cells) causes down
–– Pyruvate and Lactate regulation of glycolysis
–– Glycerol and Propionic acid TP-53 induced cancer suppressor mechanism
–– Glucogenic amino acid (most glucogenic is
Alanine)
–– Both Glucogenic & Ketogenic amino acids
–– Any TCA intermediate
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Biochemistry

Other Names:
•• Debranching enzyme → Amylo-α(1→6)-glucosidase
•• Glucan transferase → oligo-1,4-1,4-glucantransferase
or 4:4 transferase
•• Branching enzyme → amylo-(1,4→1,6)-trans
glycosylase or 1,4-alpha-glucan-branching enzyme
•• Acid maltase also called as Lysosomal acid alpha
glucosidase

HMP
•• Glucose 6–P (a hexose phosphate) is the
TIGAR- TP-53 Induced Glycolysis and Apoptosis starting material hence the name Hexose
Regulator Monophosphate Pathway

•• TIGAR decreases glycolysis, regulates •• Other name is Pentose Phosphate Pathway

apoptosis & is functionally similar to Fructose- (PPP) as Pentose Phosphate i.e. Ribose 5–P is
2,6-bisphosphatase synthesized only by this pathway.Q

Glycogen •• Produces NADPH in phase-I of HMP (irreversible

•• Stored mainly in liver & muscle and minor amount oxidative phase)Q
in brain •• Produces Ribose-5-P in phase-II of HMP
Storage Main Function End-product (reversible Non-oxidative phase)
Organ
•• It’s an anabolic pathway, thus is activated by
Liver Maintains Blood Glucose Free Glucose
Insulin & occurs in cytoplasm
Muscle Muscle contraction Glucose- 6-P
•• When muscle glycogen is used for anaerobic •• RLE → Glucose-6-P dehydrogenase (G6PD)
glycolysis, then 3 ATPs are obtained
•• Site of HMP → Liver, Lactating mammary
•• RLE for glycogenesis: Glycogen synthase, makes glands, adipose tissue, placenta, gonads & RBC.
α (1-4) bond
•• RLE of glycogenolysis: Glycogen Phosphorylase, •• Tissues which are never the site of HMP → Skin
breaks α (1-4) bond, Requires Vitamin B6, and Non-lactating mammary glands
Releases 90% of glucose in the form of glucose-
1-P •• Molecule which is intermediate as well as end
product in HMP → Glucose-6-P
•• Debranching enzyme in glycogenolysis breaks
α (1-6) bond & releases 10% of glucose in the •• Molecule which is substrate as well as product
form of D-glucose
in HMP → Glyceraldehyde-3-P
Important Information
•• Both RLE for Glycogen metabolism are Transferases
•• Both pathway of glycogen metabolism occurs in
cytoplasm
•• For Glycogen Synthesis, a Primer Glycogenin (protein) Requires
is required.
•• Enzyme common between glycolysis and glycogenesis:
Hexokinase/ Glucokinase.
•• Enzyme common between glycogenesis &
glycogenolysis: PhosphoGluco-Mutase (interconverts
glucose-1-P and glucose-6-P)
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Cerebellum Quick Revision Notes

Important Information: PREVIOUS YEAR QUESTIONS

•• Marker of Vitamin B2 deficiency: RBC Glutathione Q. Amino acid linking kreb’s cycle & urea cycle?
Reductase activityQ (NEET Jan 2019)
•• Marker for Vitamin B1 deficiency: RBC Transketolase A. Aspartate
activityQ
B. Fumarate
In G6PD deficiency C. Alanine
D. Arginine
•• Oxidative Stress is main reason for hemolysis
Exp: Aspartate serves as the precursor for
•• G6PD deficiency → ↓ NADPH production in RBC
fumarate, an intermediate in the Krebs cycle, and also
→ ↓ reduced glutathione → ↑ H2O2 → cause cell participates in the urea cycle by donating its amino
membrane lysis thus, hemolysis group.

Q. A Mediterranean person didn’t receive Primaquine. Q. All are features of gluconeogenesis except?
Which pathway gets affected by G6PD deficiency? (JIPMER Dec 2019)
A. Gluconeogenesis is synthesis of glucose from non-
Ans: HMP, as antioxidant drugs like Anti-malarials carbohydrate source
increase the oxidant stress, which further increases B. Mainly takes place in liver
H2 O 2 C. Seen in fasting state
D. Step are simple reversal of glycolysis
Sorbitol Pathway
Exp: Gluconeogenesis involves different enzymatic
reactions from glycolysis, including bypass reactions
to overcome the irreversible steps of glycolysis.

Q. Glucose is stored in Glycogen form, why? (AIIMS

June 2020)
A. Compact
•• Sorbitol accumulation in lens is responsible B. Can be reduced from multiple branches lends
for snow flake cataract in Diabetes (enzyme C. Can be stored ale multiple Sites
involved is Aldose Reductase)Q D. Can provide glucose an muchas needed and when
•• Galactitol accumulation in lens is responsible needed for 1 week
for oil drop cataract in Galactosemia (enzyme Exp: Compactness of glycogen allow storage in smaller
involved is Aldose Reductase) space as compared to equivalent glucose. Note that
400mM glucose stored as glycogen is only about 0.01
•• No cataract in HFI (Hereditary Fructose
uM.
Intolerance) because Fructose is not the
substrate for Aldose Reductase Q. Complex IV in Election Transport chain is inhibited
by? (FMGE Dec 2020)
Wilson’s disease: Copper in Descemet membrane
A. Cyanide
leads to KF (Kayser Fleischer) rings. Also, these
B. Barbiturates
patients have Sunflower cataract due to accumulation
C. Phenylnitrone
of Copper in lens
D. Malonate
Exp: Cyanide binds to and inhibits cytochrome c
oxidase, which is a component of complex IV in the
electron transport chain.

Q. Enzymes used in gluconeogenesis are? (INICET

Nov 2020)
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Biochemistry

A. Hexokinase phosphate pathway, provides a source of NADPH and

B. PEPCK ribose 5-phosphate, which are important for various
biosynthetic processes.
C. Pyruvate carboxylase
D. GLU-6 Phosphatase Q. True about Warburg effect? (NEET 2022)
E. Pyruvate kinase A. Makes cancer cells immortal
Exp: These three enzymes play key roles in the B. Aerobic glycolysis with lactate formation
gluconeogenesis pathway to bypass irreversible steps C. Produce more ATP
of glycolysis.
D. Decrease glucose uptake
Q. Enzyme present in both glycolysis and Exp: The Warburg effect refers to the phenomenon
gluconeogenesis? (AIIMS June 2020) of cancer cells preferring aerobic glycolysis over
oxidative phosphorylation, leading to increased
A. PFK lactate production.
B. PEP-CK
Q. FAD status in body is determined by? (NEET 2022)
C. Phosphoglycerate kinase
D. Pyruvate kinase A. Thiamine
B. Glutathione reductase
Exp: The common enzyme of glycolysis and
gluconeogenesis is phosphoglycerate kinase C. Hexokinase
which interconverts 1,3-Bisphosphoglycerate and D. Transketolase
3-phosphoglycerate.
Exp: Glutathione reductase is involved in the
regeneration of reduced glutathione, which, in turn,
Q. Cytochrome C oxidase is inhibited by all EXCEPT?
maintains the reduced state of FAD.
(INICET July 2021)
Q. Which of the following compound(s) is most likely
A. Methane to cause diabetic cataract: (FMGE Jan 2023)
B. H2S
A. Accumulation of sorbitol
C. CO
B. Accumulation of galactose + glucose
D. Cyanide
B. Accumulation of galactitol + glucose
Exp: Methane is not known to inhibit cytochrome c
oxidase, whereas the other options H2S, CO, and C. Accumulation of glucose only
cyanide are known inhibitors of this enzyme. Exp: In diabetes, the accumulation of sorbitol due to
increased aldose reductase activity can lead to the
Q. Glycogen phosphorylase is activated directly or development of diabetic cataract.
indirectly by? (INICET Nov 2022)
Q. Which of the following enzymes simultaneously
A. Calcium incorporates molecular oxygen and produces water?
(FMGE Jan 2023)
B. Glucose 6 Phosphate
C. Insulin A. Catalase
D. Glucose B. Cytochrome C oxidase
Exp: Calcium as Ca-Calmodulin complex directly C. Acetyl CoA carboxylase
activates glycogen phosphorylase, leading to the D. Choline esterase
breakdown of glycogen into glucose.
Exp: Cytochrome c oxidase, found in the mitochondrial
Q. The significance of HMP shunt are all except? inner membrane, uses molecular oxygen as a substrate
(INICET Nov 2022) to produce water as the final product of the electron
transport chain.
A. Source of NADPH
B. Source of ribose 5 phosphate ENZYMES
C. Source of acetyl CoA •• Enzymes are proteins except ribozyme in which
D. Utilizes ribose RNA acts as enzyme.
Exp: The HMP shunt, also known as the pentose •• Coenzymes are heat stable
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Cerebellum Quick Revision Notes

•• Enzymes are not heat stable This graph is for Simple enzymes
•• Enzymes are stereo-specific •• Michaelis-Menton constant [Km]Q
–– Km is defined as that substrate concentration
at which velocity of reaction is half of Vmax
–– Km is signature of Enzyme as it is a constant
value for a particular enzyme
–– Km does not change with change in either
enzyme or substrate concentration
–– So, in case of competitive inhibition; affinity↓
so, Km ↑

Graph between [E] & [S] for Allosteric

•• Active site: Binding Site + Catalytic site or Regulatory Enzymes
–– Serine proteases have a role in tumor cell
metastasis (e.g. Chymotrypsin, Trypsin,
elastase, plasmin, thrombin, clotting factor
10 & 11 and prostate specific Antigen)

Important Information
•• Chymotrypsin cuts at C- terminal of large
hydrophobic amino acids like Phe, Tyr and Trp
•• Trypsin cuts at carboxy terminal of basic amino acids
like Lys and Arg
•• Elastase cuts at carboxy terminal of small neutral
amino acids e.g. glycine, serine.

Enzyme Kinetics Graphs

•• Kcat → The number of Substrates converted to

product per enzyme molecule per sec

Q. Catalytic efficiency of enzyme is best expressed

by which kinetic constant?

Ans: Kcat/ KmQ

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Biochemistry

Enzyme Classification
Enzyme Class (EC no.) Distinguishing Feature
1. Oxidoreductases
•• Oxidases •• Use O2 as an electron acceptor like cyt C Oxidase
•• Dehydrogenase •• Use molecules other than O2 as electron acceptor (NAD, FAD, NADP); e.g. PDH in
link reaction.
•• Use H2O2 as electron acceptor; e.g., Glutathione peroxidase
•• Peroxidase
•• Incorporate O2 into the substrate; 2 types:
•• Oxygenase
○○ Dioxygenase: incorporates 2 atoms of molecular O2 into the substrate e.g.
homogentisate dioxygenase
○○ Monooxygenases/Hydroxylases/mixed function oxidases: incorporates 1 atom of
molecular O2 into the substrate. e.g. phenylalanine hydroxylase (converts Phe to
Tyr)
•• Reductase •• Example: Glutathione Reductase
2. Transferases
•• Methyltransferase •• Transfer one carbon units
•• Aminotransferase •• Transfer amino groups
•• Kinase •• Transfer phosphate from ATP
•• Phosphorylase •• Transfer phosphate from Pi
3. Hydrolases
•• Phosphatase •• Remove phosphate from a substrate using water
•• All digestive enzymes •• Any enzyme that breaks macromolecule e.g. amylase, maltase etc.
4. Lyases
•• Synthases •• Link 2 molecules without using ATP
•• Aldolase A & B •• Produce aldehydes via elimination reactions
•• Simple Decarboxylases •• Produce CO2 via elimination reactions
•• Hydratase •• Add or remove water but do not break bond e.g. Enolase, aconitase, fumarase, PEPCK
5. Isomerases
•• Racemase •• Interconvert L & D stereoisomers
•• Mutase •• Transfer group b/w atoms within a molecule
•• Epimerase •• Interconvert epimers
6. Ligase
•• Synthase
•• Link 2 molecule via an ATP-dependent
•• Carboxylase
•• Use ATP, Biotin and CO2 (Mn- ABC) and also uses Mg2+

•• Hydratase belongs to Enzyme category number: Enzyme InhibitorsQ

4
Type of
Km Vmax
•• Hydroxylase (Mono-oxygenase) E.C. number: 1 Inhibition

•• Hydrolase E.C. number: 3 Competitive Increased Same

Important Information Non-Competitive Same Decreased

Un-Competitive Decreased Decreased

•• Oxidases which do not require copper:
Xanthine oxidase and Sulfite oxidase
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Cerebellum Quick Revision Notes

Electrophoretic Mobility of Isoenzymes A. Competitive inhibitor

B. Non-competitive inhibitor
•• Isozyme number inversely related to mobility.
i.e. C. Allosteric inhibitor
D. Uncompetitive inhibitor
–– Least number → moves maximum
Exp: In the presence of competitive inhibitor as
–– Highest number → moves least
affinity decrease so Km changes while Vmax remains
→ In five LDH isoenzymes, LDH-1 moves max same.
and LDH-5 moves least
Q. Identify the type of inhibition? (INICET Nov
→ Out of 3 isoenzymes of CK, CK-1 moves 2022)
max and CK-3 moves least

A. Competitive
B. Uncompetitive
C. Non-competitive
D. Suicidal
Properties of Enzymes Exp: In the presence of non-competitive inhibitor
Vmax changes while Km remains same.
•• Increase velocity/rate of reaction
•• ↓ Activation energy
AMINO ACIDS & PROTEINS
•• Do not change the equilibrium of reaction
BASICS OF AMINO ACIDS
•• Do not change the free energy of substrates/
products

PREVIOUS YEAR QUESTIONS

Q. Identify the type of inhibitor in the graph?
(INICET May 2022)

•• All amino acids have one asymmetric Carbon:

BUT 2 Exceptions:
–– No Asymmetric carbon → Glycine
–– 2 Asymmetric carbons → Isoleucine &
Threonine (both are also essential amino
acids)
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Biochemistry

Important Information Classification of Amino Acids

Q. Which is Semi essential amino acid? Amino Acid Classification Based on Polarity
a. Arginine POLAR POLAR NON – POLAR
CHARGED UNCHARGED AMINO ACIDS
b. Histidine
1. Basic amino 1. Cysteine 1. Aliphatic
Ans. Both are semi essential, but arginine is more acids (Sulhydryl group) amino acids:
essential compared to histidine. So, best answer is
•• ArginineQ 2. OH – containing •• Glycine
arginine- A
•• Lysine amino acids •• Alanine
Q. Which amino acid is essential in children but not •• Histidine •• SerineQ •• Valine
in adults?
2. Acidic •• Threonine •• Leucine
Ans. Histidine amino acids •• Tyrosine •• Isoleucine
•• Glutamate 3. Amides of Acidic 2. Aromatic
Zwitterion or Ampholyte amino acid
•• Aspartate amino acids:
•• Glutamine •• Phenylalanine
•• Asparagine •• Tyrosine
•• Tryptophan
•• 3. ProlineQ
(Imino acid)
•• 4.
Methionine
•• Isoelectric pH (pl): pH at which zwitterion
# Note: There is a controversy for the polarity of
exists & at which protein precipitates out.
Tyrosine and Glycine. According to the question, one has
Protein is insoluble and has minimum buffering
to analyze what should be marked. Once you know it is
capacity.
controversy, you will be able to solve the question.
Important Information
Essential amino acids
•• Acidic amino acids have -ve charge
•• Basic amino acids have +ve charge "Any Help in Learning These Little Molecules
•• In acidic medium, Proteins & AA exist as +vely Proves Truly Valuable"
charged structures A - Arginine
•• Similarly, in basic medium, Proteins & AA exist as -vely
H - Histidine
charged structures
•• Cation → (+) I - Isoleucine
•• Anion → (-) L - Leucine
•• Cathode → (-) T - Threonine
•• Anode → (+)
L - Lysine
M - Methionine
P - Phenylalanine
T - Tryptophan
V - Valine
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Cerebellum Quick Revision Notes

Products of Amino AcidsQ Selenocysteine and PyrrolysineQ

Amino acid Products •• 21st AA → Selenocysteine → Given by UGA

Phenyl alanine Tyrosine •• 22nd AA → Pyrrolysine → Given by UAG
Tyrosine Melanin, Catecholamines, Thyroxine
•• UGA and UAG are stop codons and usually do not
Tryptophan Niacin, Serotonin, Melatonin code for any amino acid, but by Co–translational
Arginine NO, Creatine, Urea & Ornithine modification, they make Selenocysteine
Ornithine Polyamines like Putrescine, Spermidine & and Pyrrolysine (not by Post-translational
Spermine modification)
Histidine Histamine, Carnosine, Anserine
Glycine Serine, Creatine, Glutathione, Haem,
Porphyrin, Glyoxylate, Choline, Betaine,
Sarcosine

Body & urine odours in various amino acid diseasesQ

Disease Body odour
Rancid cheese/
Isovaleric acidemia
sweaty feet odour
Transamination
PKU Mousy/ Musty •• These are reversible reactions in the first step
MSUD Burnt sugar like
of catabolism of AA
Hawkinsinuria Swimming pool •• Requires B6 /PLP (pyridoxal phosphate)
Multiple Carboxylase deficiency Tom cat •• Common AA involved: Glutamate
Tyrosinemia type I,
boiled cabbage
hypermethioninemia

Tyrosinemia Enzyme defective Another name

Fumaryl Aceto Tyrosinosis/

Type I
acetate HydrolaseQ Hepatorenal
Richner Hanhart
Tyrosine syndrome/
Type II
Transaminase Oculo-Cutaneous
•• Transaminases e.g. SGOT and SGPT
syndrome
PHPP Hydroxylase •• only α-amino group can take part in transamination
/ HPPD (Hydroxy Neonatal
Type III –– Exception is δ(delta) amino group of ornithine
Phenyl Puruvate Tyrosinemia
Dioxygenase)

Important Information
•• AA having max. tendency to bind phosphate →
OH containing amino acid
•• 17 amino acids can take part in transamination
•• AA which is a site for covalent modification
→ OH containing amino acid •• 3 Amino acids that can’t take part in
transamination: Mnemonic: POLYTHENE
•• AA which is involved in O–Glycosidic bonds →
OH containing amino acid –– PO - PrOline
Q. Which AA is involved in N–Glycosidic bonds? –– LY - LYsine
Ans: Asparagine (has CONH which can provide N for –– THENE - THrEoNinE
N-glycosidic bond)
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Biochemistry

Important Information Structures of Proteins

Transport form of NH3? Name Definition
•• From body and brain – Glutamine 1° Structure Sequence of amino acids
•• From Muscles - Alanine (via Cahill cycle) Obtained from folding of 1° structure
•• α-Helix (Symmetrical / helical
2° structure structure)
•• β-Sheets
•• β-Turns (Proline & Glycine)
Further folding of 2° structure to form
3° structure
a fully folded 3° structure
> 1 polypeptide chain e.g. Hb (four
4° structure
polypeptide chains)

Monomeric protein: Those proteins which have only

one monomer. They do not have Quaternary structure
e.g. myoglobin
Important Information
AA not found in α-helix:
•• Proline and glycine → create ‘bend’ in α helixQ
•• Tryptophan → due to bulky side chain
•• Charged amino acids like Aspartate, Glutamate,
arginine, lysine

Chaperones
•• These are proteins which help in protein folding
Transdeamination: Transamination (peripheral cells) •• e.g. HSP-10 & 70, Calnexin, Calreticulin
+ Oxidative deamination (liver)
•• HSP-60 class is chaperonins
Proteins •• Calbindin is a Ca binding protein, not a chaperone
•• Protein: polymers of amino acids
•• Mostly present in RER

Important Information
•• Bonds in Enzyme-Substrate interactions
(Mnemonic: HHI)
–– H - Hydrophobic
–– H - Hydrogen
–– I - Ionic
–– Sometimes covalent but Never Van der
Note: In fats, double bond is in cis-configuration Waals Forces
•• Bonds in Protein-DNA interactions (Mnemonic:
HIV)
–– H - Hydrophobic
–– I - Ionic
–– V – Van der Waals Forces
–– Never Covalent bond
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Cerebellum Quick Revision Notes

Features 1° 2° 3° 4°
S~S Hydrophobic
Hydrophobic H-bond
Bond Covalent/ Peptide/ Amide Hydrogen bond
Hydrogen Ionic
Ionic (Mnemonic- HHI)
Functional
Absent Absent Present Present
activity

Retained because peptide

Denaturation Lost Lost Lost
bond is very strong

X-ray crystallography: Best for

Mass spectrometry,Q crystallizable proteins Q
Detection
Edman’s Technique NMR spectrometry: Best for
non-crystallizable proteins

ONE LINERS •• Beta-alanine is seen in Vitamin B5

•• Most water-soluble porphyrin – Uroporphyrin •• At pI, maximum precipitation & minimum

Buffering action
•• Least water-soluble porphyrin – Proto porphyrin
•• Most NP amino acid → Isoleucine
•• 1 gm Hb → produces 35 mg Bilirubin
•• Most Polar amino acid → Arginine
•• In DM, TCA intermediate which is depleted is
OAA (Oxaloacetate) •• Most basic amino acid → Arginine

•• In Hyperammonemia, TCA intermediate which is •• Most acidic AA → Glutamate

depleted is Alpha-ketoglutarate •• THB (Tetra Hydro Biopterin) resembles Folic
•• PHPP hydroxylase is also called as HPPD acid but it is not a vitamin
(4-Hydroxy Phenyl Pyruvate Dioxygenase) •• THB – required for the 3 aromatic AA
•• Homogentisate is also known as Di hydroxy Hydroxylases & NOS (Nitric Oxide Synthase)
Phenyl Acetate •• Segawa syndrome → def. of THB → Parkinsonism
•• Glutathione is a tripeptide made of → Glutamate, like features
Cysteine & GlycineQ •• Canavan disease → deficiency of Asparto
•• Creatine is made from 3 AA→ Arginine, Methionine acylase
& GlycineQ •• Fish odour syndrome → def. of flavin containing
•• Sources of N & C of Urea → CO2, Ammonia, Mono-oxygenase-3
Aspartate •• Edman reagent- PITC- Phenyl Iso-Thio Cyanate
•• Amino Acid linking Kreb’s and Urea cycle → •• Sanger’s reagent → 1-Fluoro 2,4 DiNitro
Aspartate Benzene (FDNB) or dinitrofluorobenzene is a
•• Amino Acid for Purines → Aspartate, Glutamine, reagent used for protein sequencing
Glycine •• While Sanger’s method is used for DNA
•• Amino Acid for Pyrimidines → Aspartate, sequencing using didexoynucleotides
Glutamine •• Vitamin required for interconversion b/w serine
•• Molecule linking Kreb’s and Urea cycle → & glycine → B6 & B9
FumarateQ •• Histidine has max. buffering capacity among all
•• Fibrinopeptide A & B are highly negatively amino acids
charged proteins made of → Aspartate & •• Histidine Side chain - imidazole ring
Glutamate
•• Tryptophan side chain - indole ring
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•• Arginine side chain - guanidino group B. Citrulline

•• Proline side chain - pyrrolidine ring C. Aspartate
D. Glycine
•• Derived amino acids: AA which do not have
codons e.g. Ornithine, Citrulline, Hydroxyproline, Exp: Arginine serves as the precursor for the
Hydroxylysine, Homocysteine synthesis of creatinine, nitric oxide (NO), and urea.

Q. Ammonia formed in brain is transported into blood

by conversion to which of following (FMGE Dec
2019)
A. Glutamine
B. Glycine
•• Vit B2 & B6 deficiency will also leads to Vit B3
deficiency C. Cysteine
D. Urea
•• Vit B3 (Niacin): Atypical vitamin (formed in the
body) Exp: Ammonia is detoxified in astrocytes by converting
it to glutamine, which can then be transported to the
•• Atypical vitamins: Vitamin D & vitamin B3 liver for further processing.

•• In carcinoid syndrome, pellagra occurs because Q. Which of the following is not used for protein
too much tryptophan used in the formation of precipitation? (INICET July 2021)
serotonin that very less tryptophan is available A. Heavy metals
for Niacin formation
B. Alcohol & acetone
C. Change in pH other than isoelectric pH
PREVIOUS YEAR QUESTION
D. Trichloroacetic acid
Q. Bends in alpha-helix structure are formed by Exp: Only at isoelectric pH, a protein has no net
which amino acid ? (JIPMER Nov 2017) charge and readily precipitate out of the solution. At
A. Glycine all other pH a protein will remain soluble in solution.
B. Lysine Q. Selenocysteine is present in which of the following
C. Methionine enzymes? (INICET Nov 2022)
D. Glutamine A. Glutathione reductase
Exp: Due to its small side chain, glycine allows for B. Glutathione peroxidase
greater flexibility and can easily accommodate the B. Thioredoxine peroxidase
conformational changes required for bends in the
D. Thioredoxine oxidase
alpha-helix structure.
Exp: Selenocysteine is an essential amino acid
Q. Which amino acid does not include post incorporated into the active site of enzymes such as
translational modification? (AIIMS Nov 2017) glutathione peroxidase
A. Selenocystiene
Q. Levels of D5 – hydroxyl indole acetic acid (5-HIAA)
B. Triiodothyronine in urine are raised: (FMGE June 2022)
C. Hydroxy-proline
A. Carcinoid syndrome
D. Hydroxy-lysine
B. Hartnup’s disease
Exp: Selenocysteine is encoded by a specific codon C. PKU
and is directly incorporated into proteins during
D. Alkaptonuria
translation, without the need for post-translational
modification Exp: Increased levels of 5-HIAA in urine are indicative
of carcinoid syndrome, a condition associated with
Q. Creatinine, NO & urea are synthesized from neuroendocrine tumors.
which, amino acid? (NEET Jan 2019)
Q. Which amino acid is not used for synthesis of
A. Arginine
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Cerebellum Quick Revision Notes

hormones? (INICET May 2023) Phospholipid (PL)

a) Tyrosine
b) Phenylalanine
c) Tryptophan
d) Glycine
Exp: While tyrosine, phenylalanine, and tryptophan
are precursors for the synthesis of various hormones
such as melatonin, serotonin etc., glycine is not
directly involved in any hormone synthesis.

LIPIDS
Classification of Lipids

Phospholipases: Enzymes which hydrolyse phospholipids

at different places

•• Base alcohol is Glycerol

Cardiolipin - a complex phospholipid

Simple Lipids
•• Phosphatidic acid = Glycerol + 2 FAs + P
•• So, product of hydrolysis of Cardiolipin = 3
Glycerol + 4 FA + 2 P
•• Can be antigenic due to its complex nature.
•• Anti-Phospholipid Syndrome - Occurs due to
Anticardiolipin antibodies. It is a thrombotic
condition and diseased female has history
of recurrent abortions. Anti-phospholipid
syndrome patients give false positive VDRL
test, as they have antibodies against cardiolipin
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Biochemistry

& VDRL test reagent has Cardiolipin antigen. Categories of PUFAs

•• Barth syndrome: Rare X-linked - so mostly Omega-3 category Omega-6 category
affecting males, Defect in cardiolipin 1. Cervonic acid/DHA 1. γ–Linolenic acid
remodelling, Cardio skeletal myopathy – muscle (DocosaHexaenoic Acid) •• 18 C & 3 =
weakness, cardiomyopathy (enlarged & weak
•• 22 C (docosa) & 6 = •• Source: oil of evening
heart), Short stature, Neutropenia leads to
(hexaenoic) primrose
Recurrent infectionsQ
•• Source: Fish oil 2. Linoleic acid
Phospholipid Types: 2. α-Linolenic acid •• 18 C & 2 =
•• 18 C & 3 = •• Source: Safflower oil
1. Glycero Phospholipids 2. Sphingo Phospholipids
•• Source: Flaxseed oil, 3. Arachidonic acid
• • Parent alcohol: •• Parent alcohol: Soybean oil) •• 20 C & 4 =
Glycerol Sphingosine 3. Timnodonic acid/EPA •• Source: Animal Fats
–– Sphingosine is an (EicosaPentaenoic Acid)
unsaturated amino •• 20 C (eicosa) & 5 =
alcohol (pentaenoic)
•• Source: Fish oil
Sphingo Phospholipids (Alcohol + FA + Phosphate)

Important information
OH OH P Choline
•• DHA
NH2 NH —FA1
○○ is required for brain development of first 2-3
Amide bond
OH OH years of life so, Health drinks are fortified with
DHA.
C18 C18 ○○ Breast milk always contains DHA.
Sphingosine
(18 C amino alcohol) Ceramide
•• α–Linolenic acid is precursor of ω-3 category means
Sphingomyelin
(present in Myelin sheet of brain) if α–Linolenic acid is taken in diet, other two ω-3 FAs
can be made form it in the body.
Glycolipids / Glycosphingolipids •• Linoleic acid is precursor of ω-6 category and can be
used to make other two ω-6 FAs in the body
•• Made of Alcohol (sphingosine) + FA + Carbohydrate
•• Most Essential FA is - Linoleic acid as it can make
Types: arachidonic acid which is required for PGs and
1. Glucosylceramide / Glucocerebroside Leukotrienes synthesis.Q

•• Never found in CNS but always found in extra •• PUFAs which are cardioprotective: ω-3 PUFAs
neural tissues Signs of Essential fatty acid (EFA) deficiency
2. Galactosylceramide/Galactocerebroside •• Generalized scaly dermatitis composed of
•• Ceramide (Sphingosine + FA) + galactose thickened, erythematous, desquamating plaques,
Acanthosis nigricans
•• Always found in CNS
•• Alopecia, Thrombocytopenia
PUFAs or Essential Fatty Acids •• Failure to thrive, Growth retardation and poor
•• ≥ 2 double bonds wound healing
•• Intellectual disability in children
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Cerebellum Quick Revision Notes

Lipoproteins
Composition of various lipoproteins

Protein/Apoprotein
Lipoprotein Lipid present
present
Chylomicron TG (exogenous) Apo B48
Chylomicron
TG + Cholesterol Apo B48 + Apo E
Remnant
VLDL TG (endogenous) Apo B100
Tangier’s disease / Familial alpha-
VLDL
lipoprotein deficiency / Hypo alpha
Remnant TG + Cholesterol Apo B100 + Apo E
(IDL)
lipoproteinemia
LDL Cholesterol Apo B100 + Apo E •• Mutation in ABCA-1 gene
Apo-A, Apo-C and •• Decreased HDL
HDL Cholesterol ester
Apo-E
•• Cholesterol accumulation in various body tissues
Like in tonsils → Large orange/yellow tonsils →
Q characteristic featureQ
• • Enlargement of throat, Liver, Spleen
(hepatosplenomegaly) and Lymph Nodes
•• Peripheral Neuropathy (Mononeuritis multiplex)

Important Information
•• Exogenous TG is transported to peripheral tissues by
Chylomicron.Q
•• Endogenous TG is transported from liver to
peripheral tissues by: VLDLQ
•• Cholesterol is transported from liver to peripheral
High density lipoproteins (HDL) tissues by: LDL
•• Cholesterol is transported from peripheral tissues to
Function- Reverse cholesterol TransportQ liver by: HDL
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Biochemistry

Important Information
Clinical Features to tackle hyperlipoproteinemia
related clinical questions
•• Tendon xanthoma → ↑ Cholesterol
•• Eruptive xanthoma → ↑ TG
•• Palmar & Tubero eruptive xanthoma → ↑ Chylo-
remnant & ↑ VLDL remnant
•• Milky plasma → ↑ Chylomicrons
•• Acute pain in abdomen [Acute pancreatitis] → ↑ TG

Ligands on lipoproteins for uptake by liver

Hyper lipoproteinemia (Fredrickson classification)Q

Type Defect LP TG Ch Common names
Lipoprotein Lipase Or Apo C-II Chylo > VLDL ↑ Normal Familial Hyperchylomicronemia
I
defect
LDL Receptor or Apo B100 ↑ LDL N ↑ Familial Hypercholesterolemia
II a

Unknown ↑ VLDL ↑ ↑ Familial combined

II b
↑ LDL hyperlipoproteinemia
apo E ↑ Chylo–remnant ↑ ↑ Broad β diseases / Dys β
III
↑ VLDL remnant lipoproteinemia

•• Neurological deficit present

Important Information
•• Other C/F → failure to thrive, diarrhoea,
Lipoprotein ‘x’
vomiting, and malabsorption of fat
•• Abnormal Lipoprotein found in two conditions:
•• Hematologic manifestations → acanthocytosis
○○ LCAT deficiency
(irregularly spiculated erythrocytes), anemia,
○○ Cholestatic states
reticulocytosis, and hemolysis with resultant
•• Rich in amphipathic lipids (PL & cholesterol) hyperbilirubinemia.
•• Poor in neutral lipids (TG & cholesterol ester)

Abetalipoproteinemia, or Bassen-
Kornzweig syndrome
•• A stands for Absent (or negligible) beta-
lipoproteins - VLDL , IDL and LDL
•• defective assembly and secretion of (apo)
B-containing lipoproteins → Apo B 48 & Apo B Fatty Acid Synthesis
100
•• Mutation in Microsomal Triglyceride Transfer
Protein - MTP (transfers TGs from intestine &
liver to Chylomicrons & VLDL)Q
•• Decreased plasma TGs (not absorbed from
intestine)
•• Defective absorption of fat-soluble vitamins as
chylomicrons not formed
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Cerebellum Quick Revision Notes

FA synthase complex - Main enzyme of fatty acid & also in muscles but never occurs in liver, due
synthesis: a multienzyme complex & has 2 monomers to absence of Thiophorase in liver. Q
Important Information
Q. FA is synthesized from?
Ans: Acetyl CoA and not malonyl CoA
•• Because extra Carbon of Malonyl CoA is not
getting added in newly synthesized FA
•• 1st enzyme carboxylase adds one CO2 to form
malonyl CoA but 2nd enzyme FA synthase
removes the CO2. So, only CO2 of acetyl CoA
are used.
•• But, Main Donor of carbon for fatty acid
synthesis – Malonyl CoA
Important information
•• Thiolase is a common enzyme for 4 lipid
metabolic pathways:
1. Ketone body synthesis
2. Ketone body utilization
3. Cholesterol synthesis
4. β-oxidation of FA

Types of Hypoglycemia
Ketotic-hypoglycaemia Non-ketotic hypoglycaemia
Von Gierke’s Disease Insulinoma

Alcoholism Any defect in β-oxidation e.g.

MCAD deficiency, Jamaican
vomiting sickness, Carnitine or
CPT-I or CPT-II deficiency
Starvation Defects in KB pathway

Important Information on Lipids

Lipids Functions
•• Role as lung surfactant
Phosphatidyl choline/ •• Deficient in preterm infants
Lecithin (Di palmitoyl with RDS (Respiratory
phosphatidyl choline)
Distress Syndrome) Q
Phosphatidyl •• A structural phospholipid in
ethanolamine/ brain also has a role in blood
Cephalin clotting
•• Role in cell cycle signalling in
Phosphatidyl Serine
relation to apoptosis

•• KB synthesis occurs only in Liver whereas KB

utilization occurs in vital organs (Brain & Heart)
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Biochemistry

•• Role in signal →Thiophorase

transmission across •• Immediate precursor of acetoacetate → HMG
membrane, CoA
Phosphatidyl Inositol
•• Also serve as a reservoir •• Carnitine def. → Muscle breakdown & pain,
of PG synthesis, as it myoglobinuria, hypotonia, Poor exercise
has Arachidonic acid intolerance, Increased CK-MM
•• Present in myelin sheath has
•• Lanosterol is the first steroid or first cyclic
Sphingomyelin structural role in lipid raft & compound formed in cholesterol synthesis
cell signalling
•• MCAD deficiency → Non ketotic hypoglycemia
•• Its carbohydrate
portion act as antigenic & dicarboxylic acidosis Q
Glycolipid/ determinant for Blood •• LCAD or LCHAD deficiency (Long-chain
Glycosphingolipid group Ag & Cell surface 3-hydroxyacyl-coenzyme A dehydrogenase) →
receptor for cholera, in acute fatty liver of pregnancy Q
tetanus & botulinum.

PREVIOUS YEAR QUESTION

One liners
Q. Active metabolite form in synthesis of fatty acid
•• Cholera toxin binds oligosaccharide portion of
is? (AIIMS Nov 2017)
GM1 ganglioside receptor. Q
A. Acetyl CoA
•• Tetanus and botulinum toxins selectively bind
B. Malonyl CoA
gangliosides of the G1b series, namely, GT1b,
GD1b, and GQ1b. C. Stearate
D. Palmitate
•• Treatment in Gaucher’s → Acid glucosidase →
Imiglucerase, Velaglucerase alpha, Taliglucerase Exp: Malonyl CoA is the active metabolite in the
alpha synthesis of fatty acids as it serves as active acetyl
CoA donor in fatty acid synthesis.
•• First intermediate of LOX pathway → HPETE
(Hydro Peroxy Eicosa Tetra Enoic acid) Q. Major product of fatty acid synthesis is? (AIIMS
•• First step in the synthesis of eicosanoids Nov 2017)
(prostaglandins & leukotrienes) → hydrolysis by A. Acetyl CoA
Phospholipase A2, to release arachidonic acid. B. ATP
•• Primary prostaglandins are PG-E2, PG-D2 & PG- C. Citrate
F2 alpha D. Palmitate
•• Many patients of Retinitis pigmentosa have Exp: Palmitate is the major product of fatty acid
decreased DHA (Docosa Hexaenoic Acid) levels synthesis and serves as the starting point for the
•• Apolipoprotein responsible for Alzheimer dis → synthesis of longer fatty acids
Apo E4
Q. Which of the following is an essential fatty acid?
•• Citrate activates Acetyl CoA carboxylase (FMGE JUNE 2018)
•• Acyl carnitine is the intermediate formed in the A. Citric acid
transport of fatty acids through mitochondrial B. Linoleic acid
membrane via Carnitine.
C. Stearic acid
•• Starting point of ketone body synthesis → D. Palmitic acid
Acetyl CoA
Exp: Linoleic acid is an essential fatty acid that cannot
•• First enzyme of ketone body synthesis → be synthesized by the body and must be obtained
Thiolase from the diet.
•• First enzyme of ketone body utilization
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Cerebellum Quick Revision Notes

Q. Type I hyperlipoproteinemia is characterized by? Exp: Fatty acid transport through the mitochondrial
(NEET Jan 2019) membrane is facilitated by carnitine, which helps
transport long-chain fatty acids into the mitochondria
A. Elevated LDL
for beta-oxidation.
B. Elevated HDL
C. Elevated lipoprotein lipase Q7. For Coronary artery prevention, which needs to
be given: (FMGE Jan 2023)
D. Elevated chylomicrons.
A. Saturated fatty acid
Exp: Type I hyperlipoproteinemia is characterized by
elevated levels of chylomicrons (large triglyceride- B. Omega 3 FA
rich lipoproteins) due to deficiency of enzyme LPL C. Omega 6 FA
which breaks down TG in chylomicrons. D. Omega 9 FA
Q. Ketone bodies are not utilized by? (JIPMER May 2019) Exp: Omega-3 fatty acids, such as eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA), are
A. Brain
recommended for coronary artery prevention due to
B. RBC their beneficial effects on heart health.
C. Heart
Q. Liver produces KB but cannot use KB due to absence
D. Skeletal muscle
of which enzyme: (INICET May 2023)
Exp: Red blood cells do not have mitochondria and,
A. Thiophorase
therefore, cannot utilize ketone bodies for energy.
B. Thiolase
Q. A patient has multiple tendon xanthomas. Serum C. HMG CoA synthase
cholesterol (398 mg/dl) & LDL (220 mg/dl) were found
D. HMG CoA Reductase
to be raised. Statins were given to this patient. What
is the diagnosis? Exp: The absence of thiophorase enzyme (first enzyme
(NEET Sep 2021) of KB utilization) in the liver prevents the utilization
of ketone bodies produced by the liver.
A. Lipoprotein lipase deficiency
B. Familial hypercholesterolemia Q. A patient with C/O muscle weakness came to OPD.
C. Tangier’s disease Doctor found he has cardiomyopathy & diagnosed him
to be a case of Barth syndrome, where patient has
D. Huntington’s disease
mitochondrial dysfunction. What is the defect in this
Exp: The presence of tendon xanthomas, along with patient: (INICET May 2023)
elevated serum cholesterol and LDL levels, suggests a
A. Cardiolipin
diagnosis of familial hypercholesterolemia
B. Lecithin
Q. Eicosanoids are formed from? (INICET May 2022) C. Lysolecithin
A. Arachidonic acid D. Cephalin
B. Platelet aggregation Exp: Barth syndrome is characterized by a defect in
C. 4 fused rings the synthesis of cardiolipin, a phospholipid primarily
D. Arginine found in the inner mitochondrial membrane
Exp: Eicosanoids, such as prostaglandins and
leukotrienes, are derived from arachidonic acid, which MOLECULAR BIOLOGY
is an omega-6 fatty acid
Nucleic Acid
Q. Fatty acid transport through mitochondrial
•• Nucleic Acid (DNA/RNA) = Polymer of
membrane is via? (NEET PG 2022)
Nucleotides
A. Carnitine
•• NucleoTide = Nitrogenase base + Sugar +
B. Acyl carrier protein
Phosphate
C. Cholesterol transporter
•• NucleoSide = Nitrogenase base + Sugar
D. LCAT
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Biochemistry

•• So, Nucleotides = Nucleoside + Phosphate NITROGENOUS BASES

•• Purine - Adenine (A) & Guanine (G) 1. Purines
•• Pyrimidines – Uracil (U), Thymine (T) and
Cytosine (C)
•• DNA → Bases are A, T, C, G
•• RNA → Bases are A U, C, G

Nitrogenous Base
N–base Nucleoside Nucleotide form

AMP, ADP, ATP, dAMP, dADP,

Adenine Adenosine 2. Pyrimidines
dATP
GMP, GDP, GTP,
Guanine Guanosine
dGMP, dGDP, dGTP
CMP, CDP, CTP, dCMP, dCDP,
Cytosine Cytidine
dCTP
UMP, UDP, UTP
Uracil Uridine
(deoxy forms not available)
dTMP, dTDP, dTTP
Thymine Thymidine
(ribose forms not available)

Ribose to Deoxyribose conversion occur Tip to remember: Thymine matching with Methyl
at Di-Phosphate level Note: Thymine (Pyrimidine) is different from
Thiamine (Vitamin B1)

Source of C & N atoms of Purine and

Pyrimidines

Uracil to Thymine conversion

•• Occurs at the level of Mono-Phosphate i.e.
UMP→TMP
•• CH3 group is added from THF (Tetra Hydro
Folate) Thymine
•• Enzyme involved: Thymidylate Synthase THF
Glutamine O
Uracil to cytosine conversion at tri- 4 CH3
H N3 5
Phosphate level
2 1 6
•• Occurs at level of triphosphate i.e. UTP → CTP O N
Aspartate
•• NH2 group provided by glutamine CO2 H
•• Enzyme involved: CTP Synthetase
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Purine Pyrimidine removal of amino group

N1 Aspartate N1, C4, C5, Aspartate •• Important in B & T Lymphocytes
C6 –– if ↑ ADA → Suggestive of TB
N3, N9 Glutamine N3 Glutamine
–– if ↓ ADA → Leads to Severe Combined
Immunodeficiency (SCID)
C4, C5, N7 Glycine C2 CO2
Lesch Nyhan SyndromeQ
C6 CO2 Extra CH3 THF •• Complete deficiency of HGPRT
C2, C8 THF
•• Gout d/t ↑ ↑ Nitrogenous bases → ↑ ↑ Uric acid
•• Self-mutilation d/t ↑ PRPP (neurotoxic)
Important information
Product of catabolism of N-bases
Kelly Seegmiller Syndrome
•• Partial deficiency of HGPRT
Purines Uric Acid (Soluble)
Pyrimidines CO2, NH3, β-Alanine
•• Only gout present but no neurological problems
Thymine CO2, NH3, β-Amino PYRIMIDINE SYNTHESIS
isobutyrate

PURINE SYNTHESIS
1.De novo pathway
•• High energy consuming pathway (15-20 steps)
•• RLE: PRPP glutamyl amido transferase

2. Salvage pathway
•• Less energy consuming pathway (only 1 step)
•• Main enzyme: HGPRT (Hypoxanthine Guanine
Phosphoribosyl Transferase)

PURINE CATABOLISM

OPRT + Decarboxylase
•• Bi-functional enzyme (single protein with 2
enzymatic activities)
Q
•• Deficiency leads to Orotic Aciduria

Orotic aciduria
•• Growth Retardation and developmental delay
–– Neurological defects
Adenosine Deaminase (ADA)
–– Megaloblastic anaemia which is non-
•• Used for conversion of adenosine to Inosine by responsive to B12 or folic Acid Rx
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Biochemistry

•• Rx: Give only Uridine as other pyrimidines can be Centromere

synthesized from it Chromosome Diagram Example
Position
Centre Metacentric Primitive,
SUGAR
Chr 1,3
1. Ribose

Near the Submetacentric most of human

centre autosome & X
chr

Close to end Acrocentric Y chr

and some
autosomes
(13, 14, 15,
21, 22)
At the end Telocentric Not present
in human
2. Deoxyribose
BARR BODIES
•• Inactive condensed X chromosome
•• Number of Barr Bodies = No. of X chromosomes
-1Q
No. of
Genotype Barr Phenotype
Bodies

Normal Male XY 0 Normal

Normal
XX 1 Normal
female
•• Formed by removal of one O atom of OH at 2 nd
Turner Female with no
position carbon of ribose XO 0
Syndrome Barr body
•• But If oxygen is removed from both 2’ & 3’ Klinefelter’s Male with Barr
position, then it is called 2’-3’ dideoxyribose. XXY 1
Syndrome body
If this is used, it will stop DNA synthesis as
Female with two
free 3’ OH is lost, which is required to add next Super Female XXX 2
Barr bodies
nucleotide in a growing DNA/RNA chain

CHROMOSOMES ABSORPTION OF UV-LIGHT

•• 23 chromosomes = 22 Autosomes + 1 sex •• Due to conjugated double bonds present in the
chromosome ring.
•• Nucleic acids absorb UV light at 260 nm due to
Haploid state (n) Diploid state (2n)
Nitrogenous bases.
•• 23 chromosomes •• 23 pairs of chromosomes
•• This absorption is more for Purines as compared
•• Present in Germ Cells •• Present in somatic Cells to pyrimidines.

Types of chromosome - Depending upon position of •• Amino acids and proteins also absorb UV light
at 280 nm
centromere
–– It is due to aromatic amino acids
–– maximum for tryptophan Q
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Cerebellum Quick Revision Notes

•• NAD and NADP absorb light at 340 nm Palindrome definition: same sequence on both strands
(when read in 5’ to 3’ direction)
•• Porphyrin absorb at 400 nm (Soret Band)

Due to conjugated
DNA REPLICATION
Absorption of
Molecule double bonds in the Enzymes of DNA replication
light at:
rings
1. Helicase: Causes strand separation, Use ATP,
DNA 260 nm (UV) Nitrogenous bases Creates positive supercoils
Aromatic amino 2. Topoisomerase- Relieve positive supercoils
Proteins 280 nm (UV) acids (maximum by
tryptophan) 3. Single Strand DNA Binding Proteins (SSBs)-
Prevents reannealing by binding single DNA
NAD/NADP 340 nm (UV) Adenine strands in prokaryotes.
Porphyrins 400 nm (Visible) Pyrrole rings
Note: Helicases, Topoisomerases & SSBs
BONDS IN DNA constitute Unwinding proteins
4. Primase
•• Synthesizes the primers (RNA primer) using
DNA as Template
–– 1 primer is required for leading strand
–– Multiple primers are required for lagging
strand

DNA
•• Right-handed
•• ds in both Prokaryotes and Eukaryotes
–– Prokaryotic DNA is circular (two ends are
joined to form closed circle)
–– Eukaryotic DNA is linear (two ends are free) 5. DNA Polymerase III- Synthesizes both leading
•• Eukaryotic nuclear DNA has introns that & lagging strands
prevents mutations 6. DNA Polymerase I
•• But eukaryotic mitochondrial DNA is like •• Removes RNA primers from both leading &
prokaryotic DNA with no introns, so there are lagging strands
more chances of mutation in it.
•• Fills gap only on lagging strand
Palindrome •• Creates a single gap on leading strand
Q. Which of the following is a palindrome? 7. DNA Ligase- Creates 3’-5’ Phosphodiester bond
A. TAAT to join DNA with DNA, Uses ATP & acts only on
lagging strand
B. GGCC
Ans: B
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Biochemistry

Prokaryotic vs Eukaryotic DNA Polymerase

E. coli (Prokaryotic) Eukaryotic Function

DNA Pol I Nucleus Mitochondria

RNase H RNase H
FEN-1 FEN-1 (Flap Remove primer and fill the gapQ

δ−polymerase (minor role) endonuclease)

DNA Pol II DNA proof reading and repairQ

β DNA repair

γ Mitochondrial DNA synthesis

DNA Pol III ε Leading strand

δ Lagging strand

DNA-G α Primase

Mnemonic for DNA polymerases •• Lεading (γ) → ε-Polymerase

•• gaMMa (γ) → Mitochondrial Q
•• LAδδing → δ-polymerase

Proof reading Repair

Correction •• Correction during synthesis •• Correction after synthesis
Enzymatic activity •• Mostly endonuclease activity
•• 3’ → 5’ Exonuclease activity
•• Sometimes 5’ → 3’ Exonuclease activity
Enzyme in prokaryotes •• DNA Polymerase II •• DNA Polymerase II

•• All Polymerases except α & β •• β polymerase (main)

Enzyme in eukaryotes
polymerase •• ε polymerases (minor role)
Phase of cell cycle •• Occurs in S phase •• Most repairs occur in G1 phase

Somatic cells •• Gap of leading strand is filled by Telomerase

•• Have limited number of divisions due to the gap 4. Telomerase

present in leading strand
•• Protein with RNA attached to it (a
–– The gap left with each cell division leads to Ribonucleoprotein)
telomere shortening, so cell has limited
divisions. •• RNA acts as template on which DNA is
synthesized
TELOMERE •• Not a Ribozyme as RNA do not act as enzyme,
•• Ends of chromosome instead RNA acts as a template to synthesize
DNAQ
•• Has (TTAGGG)n sequence repeated ‘n’ no. of
timesQ •• RNA dependent DNA polymerase (Reverse
Transcriptase)
–– Telomere Shortening is responsible for aging
& death •• Activity increases in cancer & decreases with
aging
Germ cells/Stem cells
•• Have infinite number of divisions
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DNA REPAIR
Type of repair Cell cycle phase Damage Cause Disease
Nucleotide excision repair G1 T-T dimers UV radiation damage Xeroderma pigmentosaQ
Spontaneous, heat, IR
G1 mainly but can C → U conversion Rare, MUTYH associated
Base excision repair rays, viral infection,
occur in any phase by deamination polyposis
Nitrous oxide
HNPCC (Hereditary
Mismatch repair G2 Mismatched base Proofreading error Non-Polyposis Colorectal
Cancer)Q

TRANSCRIPTION RNA (see fig)

•• Formation of RNA from DNA as template in •• Sense strand: as it has same sense of direction
nucleus as new RNA (see fig)

•• Enzyme of transcription: DNA dependent RNA

polymerase Q

RNA polymerase Holoenzyme (complete

enzyme)
•• 5 subunits: 2α, β, β’, ω, σ
Subunits Function
α, ω Enzyme assembly
β main catalytic subunit
β’ Template (DNA) binding
σ Initiation of transcription (recognize promoter)

Types of RNA polymerase

RIBOZYMES
1. In Prokaryotes, only single type present
•• Ribozyme means RNA acting as enzyme
2. In Eukaryotes
Eukaryotic RNA polymerase
RNA synthesized
types
Type I All rRNA except 5S RNA
mRNA, miRNA, lncRNA
Type II
few snRNA & snoRNA
tRNA, 5S rRNA,
Type III
few snRNA & snoRNA

Mitochondrial RNA Polymerase Mitochondrial RNA

Note: Telomerase is not a Ribozyme; RNAase H is not

Template / Anti Sense / Non-Coding / a Ribozyme
Minus Strand Codons
•• Template strand: as new RNA is getting •• Nucleotide Triplets e.g. ACG → 3 bases make 1
synthesized using this strand as template codon
Non-Template / Sense / Coding / Plus •• 4 bases are used to make codons: A U C G
Strand •• 43 = 64 codons combinations are possible
•• Coding strand: as it has the same codons as new
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Q. If 4 bases make 1 codon, then how many codons are –– Misnomer i.e. name indicates that it helps in
possible? release. However, it does not help in release.
It only recognises the stop codon
Ans: Total 44 = 256 codons are possibleQ
•• Peptidyl transferase releases the polypeptide
•• Out of 64, 3 are stop codons i.e. do not code for from P site
amino acids
1. UAA Important Information

2. UAG Q. How many ATP & GTP are used to add one AA in
the growing polypeptide chain
3. UGA
Ans:
•• So, for 20 AA, 61 codons are present
2 ATPs → for the activation of AA
–– or on an average, for each amino acid 3 codons
are present 2 GTPs → 1 GTP used in elongation for adding AA

–– Each amino acid has more than 1 codon, known → 1 GTP used for translocation
as Degeneracy/Redundancy of codon So, 4 high energy phosphates are used to add one
•• AA that do not show degeneracy (only 1 codon AA in the growing polypeptide chain
present):
Crispr-CAS 9 System
1. Methionine - AUG
•• CRISPR-Clustered Regularly Interspersed
2. Tryptophan – UGG Short Palindromic Repeats

Translation •• CAS-9 – a CRISPR associated endonuclease

–– It will cause a double strand DNA break
Activation of AA/charging of
tRNA - occurs before Initiation •• Cheap and easy method to cut the DNA at
desired place
•• It is an immune system in bacteria against
bacteriophages
–– Memory of bacteriophage infection and
immunity is transferred to future generation
also, So protects many future generations
Amino Acyl tRNA Synthetase from viruses

•• Have 20 isoenzymes (one for each AA) PCR (Polymerase Chain Reaction)
•• Is the only point of proofreading during Used for amplification of DNA
translation
Components of PCRQ
•• Responsible for fidelity/accuracy of protein
synthesis 1. Heat is used for denaturation and 2 strands
separation
Factors in translation in prokaryotes &
2. DNA to be amplified
eukaryotes
3. 2 primers (1 for each strand)
Prokaryotes Eukaryotes
Initiation IF 1, 2, 3 eIF 1, 2, 3, 4F (RL) 4. Enzyme: Taq polymerase [derived from Thermus
aquaticus bacteria]
Elongation EF– Tu, Ts, G eEF 1α, 1β, 1γ, eEF2
Termination RF 1, 2, 3 eRF 5. Substrates: Deoxyribonucleotides
Factors used in translocation: EF-G (Prokaryotic) 6. Mg2+ in Buffer
and eEF-2 (Eukaryotic) Note: Dideoxyribonucleotide is never the component
•• Releasing factor (RF) of PCR
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Real Time PCR / Quantitative PCR Disorders caused due to genomic imprinting
•• Normal PCR is End-PCR i.e. only at the end of 1. Prader Willi Syndrome (PWS)Q
whole PCR process, we get the products and do
•• Paternal allele is deleted, and Maternal allele is
the analysis.
imprinted/inhibited means both copies (father
•• Real time PCR displays the amount of DNA and mother) of gene not working giving rise to
synthesized in real time, as it has SYBR-green sign and symptoms
dye , which gives fluorescence when bound to
the synthesized ds-DNAQ 2. Angel Man syndromeQ
•• Maternal copy of allele is deleted, and Paternal
RT-PCR (REVERSE TRANSCRIPTASE PCR)
allele is imprinted/inhibited leading to various
sign and symptoms

MICRO ARRAY/chip

GENOMIC IMPRINTING
•• It is gene inhibition at the level of transcription
Lot of DNA fragments (probes) are placed on a small
Mechanisms of Genomic Imprinting material looking like a chip.
1. DNA methylation- most common mechanismQ
Uses of chip
•• occurs at CG site/CG Island/CpG sites (C & G •• Can detect multiple mutations
together present on same strands)
•• Can do multiple gene expression analysis
•• cytosine is usually methylated in CG site that
causes inactivation of the gene •• Can do comparative genomic hybridization
•• Can detect SNPs (single nucleotide
polymorphisms)

Limitation
•• Can’t detect aneuploidy (monosomy & Trisomy)

Karyotyping
•• Best technique for detecting monosomy &
•• DNA methylation can be detected by Na- trisomy
bisulfite method •• Limitations
2. PTM of Histones (Post Translational Modifications) –– Lengthy (culture of cell required)
•• Histone Deacetylation –– It can only be done in metaphase arrest
•• Histone Methylation –– Cannot detect micro deletions, amplifications
•• Method to detect PTMs: Chromatin Immuno and complex translocationsQ
Precipitation (ChIP)
Fish (Fluorescent In Situ-
Hybridization)
•• Advantages
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–– Can detect aneuploidy If there is no male to male

X-linked
–– Can be done in any phase of cell cycle transmission
More males are affected,
–– Rapid (result in 24 hours)
and affected son born to X-linked recessive
–– Tells gene location on chromosomes unaffected mother (carrier)
–– Can detect microdeletion, amplification and
complex translocationQ KLENOW FRAGMENT
Classical /Mendelian Inheritance It is the larger fragment towards the ‘C’ terminal in
Disorders DNA Polymerase I, which is lacking 5’ → 3’ exonuclease
activity
AD (Autosomal Dominant)
•• Familial hypercholesterolemia

AR (Autosomal Recessive)
•• Most of biochemical enzyme defects
•• All MPS disorders except Hunter
•• All urea cycle disorder’s except OTC
•• All sphingolipidoses except Fabry’s disease
•• All amino acid disorders e.g. PKU, Albinism, HCU
etc Severity of damage in point mutation
•• All glycogen storage disorders Frameshift > Non-Sense > Missense

•• Orotic aciduria •• Frameshift Mutation: when insertion or deletion

is not in multiple of 3
•• Wilson’s disease
–– Whole codon reading frame is shifted leading
•• ADA deficiency to misreading of entire gene
•• Hemochromatosis •• Missense mutation: AA changed

X-linked Recessive •• Non-sense Mutation: Insertion of stop codon

•• Menke’s Disease Methylation has role in DNA

•• Lesch Nyhan Syndrome •• DNA Replication & Transcription
•• Mismatch repair
•• G6PD deficiency
•• X-chromosome inactivation
Important pointers to determine inheritance
•• Chromatin remodelling or chromosome
patterns segregation (heterochromatin formation)
If both male & female
RNA
are affected with equal Autosomal disorder
frequency •• Splicing, Alternate splicing and regulation of
splicing
If atleast one parent is
Dominant disorder
affected •• 7-methyl guanosine cap in mRNA
If neither of parent is •• Gene regulation or regulation of gene
Recessive disorder
affected expression - Gene silencing & Genome imprinting
If all sons are affected Y-linked (Epigenetics)
If affected mother to all •• Others: Embryonic development, Maintenance of
Mitochondrial Inheritance genome stability, Carcinogenesis, Atherosclerosis,
offspring
ageing, Exercise, B-cell differentiation
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Gene transfer methods: ONE LINERS

•• Transformation – transfer of naked DNA •• We always read in 5’ to 3’ direction.
from environment or dead bacteria to a living
bacterium •• Synthesis of DNA & RNA occurs in 5’ to 3’
direction.
•• Transfection – transfer of DNA into eukaryotic
cell deliberately •• Centromeres are made up of satellite DNA
repeats.
•• Transduction – transfer of DNA & RNA through
virus, called bacteriophage •• Banding technique for dicentric chromosomes-
C-bandingQ
•• Conjugation – by cell to cell contact, formation
of pilus in donor bacteria to recipient bacteria •• TATA box is rich in A & T
•• Lipofection – when liposome used (liposome can •• Shine Dalgarno is rich in A & G
carry DNA or drugs)
•• Telomeres are rich in T & G
•• Rifampicin inhibits Prokaryotic RNA Polymerase
•• Amanita phalloides – a wild mushroom, also
known as mushroom death cap, produces toxin:
alpha-Amanitin, which inhibits Eukaryotic RNA
Polymerase
•• Deamination of methylated cytosine will form →
ThymineQ
•• Apo B48 is synthesized from ApoB 100 gene
Operon in Prokaryotes in intestine by process: RNA editing (Post
transcriptional modification)Q
Lac operon Tryptophan operon
•• Vitamin deficiency which can lead to the
•• Inducible (Lactose •• Repressible (Trp is co-
presence of Uracil in the genetic code- FolateQ
is the inducer) repressor)
•• Catabolic system •• Anabolic system •• Methotrexate (an antimetabolite) inhibits
enzyme dihydrofolate reductase, so it inhibits
•• Usually off •• Usually on (inactive when
the synthesis of the purines and pyrimidines
high trp is present)
Rasburicase
•• 3 structural genes- •• 5 structural genes (A, B,
Z, Y & A C, D & E) –– a recombinant form of an enzyme, urate
oxidase.
•• Repressor protein •• Repressor protein is
is active inactive –– rapidly reduces existing hyperuricemia in
•• Turned on when •• cAMP is not necessary tumor lysis syndrome.
glucose decreased, here
–– It converts hypoxanthine and xanthine into
cAMP increased &
allantoin, a more soluble molecule, easily
Lactose present
cleared by kidneys.
•• Werner syndrome/Adult Progeria: patients
Important Information have accelerated telomere shortening with
•• DNA replication & repair occurs in 5’ to 3’ damaged DNA & loss of helicase, so premature
direction. ageingQ
•• DNA proofreading occurs in 3’ to 5’ direction.
•• Transcription occurs in 5’ to 3’ direction. PREVIOUS YEAR’S QUESTION
•• RNA Editing is directional, from 3’ to 5’, along Q. Which of the following does not favor permissive
an unedited RNA.
euchromatin due to changes occurring at cytosine
•• tRNA & rRNA are stable, so no cap or tail is residues at CpG islands in DNA? (AIIMS May 2018)
required.
A. Methylation
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Biochemistry

B. Phosphorylation Exp: Poly A polymerase is an enzyme involved in the

C. Alkylation addition of poly(A) tails to the 3’ end of messenger
RNA (mRNA) molecules. It is not a ribozyme but is a
D. Sumoylation
protein enzyme.
Exp: Methylation of cytosine residues at CpG islands
in DNA leads to the formation of heterochromatin, Q. In CRISPR – Cas 9 System, which repair mechanism
which is associated with gene silencing rather than is used for genome editing? (NEET Nov 2019)
permissive euchromatin. A. Non homologous end repair
Q. The enzyme deficient in Lesch Nyhan syndrome B. Homologous repair
is? (NEET May 2018) C. Mismatch repair
A. Adenosine Deaminase D. Nucleotide excision repair
B. PRPP synthetase Exp: The CRISPR-Cas9 system most often uses the
C. HGPRTase non-homologous repair mechanism for genome editing,
where a desired DNA sequence is inserted using a
D. Xanthine oxidase
template.
Exp: HGPRTase, or hypoxanthine-guanine
Phosphoribosyltransferase (main enzyme of Q. Restriction endonuclease will act on which of the
salvage pathway) is the enzyme deficient in Lesch- following? (AIIMS Nov 2019)
Nyhan syndrome. A. AAGCTT
Q. Which is incorrect about DNA polymerase - I? B. AAGAAG
(NEET May 2018) C. TACGAG
A. Not required in bacteria D. GAGAGG
B. Role in primer removal Exp: Restriction endonucleases cleave DNA at
C. Fill gaps between okazaki fragments palindromic sites (sites with same DNA sequence
on both strands when read in 5’-3’ direction), and
D. Involved in DNA replication
AAGCTT is a palindromic site.
Exp: DNA polymerase I is required for various
functions in bacteria, including primer removal, Q. Amino acid which absorbs UV light at 280 nm?
filling gaps between Okazaki fragments during DNA (NEET Jan 2020)
replication A. Tryptophan
Q. True about DNA polymerase III? (NEET May B. Histidine
2018) C. Aspartate
A. Required for translation D. Ornithine
B. Has DNA repair function Exp: Tryptophan absorbs UV light at a wavelength of
C. Forms okazaki fragments & needs RNA primer 280 nm, which is commonly used to quantify proteins
using the absorbance at this wavelength.
D. Has no proof-reading activity
Exp: DNA polymerase III is responsible for Q. PCR steps are? (INICET Nov 2020)
synthesizing the leading and lagging strands during A. Denaturation, annealing, elongation
DNA replication, including the formation of Okazaki
B. Annealing, denaturation, ligation
fragments, which require an RNA primer.
C. Ligation, denaturation, annealing
Q. Which of the following is not a Ribozyme? (NEET D. Denaturation, annealing, elongation, hybridization
Jan 2019)
Exp: The steps of PCR (polymerase chain reaction)
A. Transpeptidase include denaturation of DNA, annealing of primers,
B. Ribonuclease and elongation by DNA polymerase.
C. Peptidyl transferase
Q. A patient has swelling in MCP joints. Serum uric
D. Poly A polymerase acid levels were raised. Doctor will prescribe medicine
against which enzyme? (FMGE Aug 2020)
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A. Thymidylate synthase D. Gene body

B. Xanthine oxidase Exp: The binding site of miRNA (microRNA) on mRNA
C. ADA (Adenosine Deaminase) is typically located in the 3’ untranslated region (UTR)
D. HGPRT of the mRNA.

Exp: In a patient with swelling in MCP joints and Q. Which of the following methods uses RNA?
elevated uric acid levels, the enzyme xanthine (INICET July 2021)
oxidase, which converts hypoxanthine and xanthine to
A. Western blot
uric acid, is targeted for treatment.
B. RT-PCR
Q. Mother side uncle has disease... Her son has C. Sangers method
disease. Which type of inheritance is this? (FMGE
D. G-banding
Aug 2020)
Exp: Reverse transcription polymerase chain reaction
A. X-linked recessive
(RT-PCR) is a method that uses RNA as a template
B. X-linked dominant to synthesize complementary DNA (cDNA), which is
C. Autosomal dominant then amplified by PCR.
D. Autosomal recessive
Q. Deamination of methylated cytosine will form?
Exp: In X-linked recessive inheritance, there is (INICET May 2022)
no male to male transmission, but more males are
A. Uracil
affected, and affected son is born to unaffected
mother (carrier). B. Guanine
C. Adenine
Q. All are true about telomerase EXCEPT? (INICET
D. Thymine
Nov 2020)
Exp: Deamination of methylated cytosine results in
A. has reverse transcriptase activity
the conversion of cytosine to thymine.
B. Maintains fidelity of DNA replication
C. Maintains length of DNA Q. Banding technique used for dicentric chromosomes?
(INICET May 2022)
D. Found only in eukaryotes
A. G
Exp: While telomerase has an important role in
maintaining the length of telomeres and compensating B. NOR
for their shortening during DNA replication, it does C. C
not maintain the fidelity of DNA replication which is D. R
mainly done by DNA pol I and III.
Exp: C banding stains heterochromatin which are regions
Q. RNAi acts through? (INICET July 2021) of the chromosomes at or near centromere. So, C banding
will be most useful for dicentric chromosomes.
A. Knock out
B. Knock down Q. DNA-Protein interactions can be studied by using?
C. Knock in (INICET May 2022)
D. Knock up A. DNA fingerprinting

Exp: RNA interference (RNAi) acts by reducing or B. DNA footprinting

“knocking down” the expression of specific genes by C. Northern Blotting
degrading mRNA produced from that gene. D. ELISA

Q. Binding site of miRNA on mRNA? (INICET July Exp: DNA footprinting is a technique used to study
2021) DNA-protein interactions by identifying regions of
DNA protected by protein binding.
A. 5’ UTR
B. 3’ UTR Q. dd-NTPs in Sanger’s Sequencing technique uses?
C. Gene promotor (INICET May 2022)
A. Its fluorescence
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B. DNA polymerization D. GUAGAUC

C. Termination of polymerase Exp: The base sequence of the RNA product
D. Removal of primer synthesized from the given DNA template sequence
GATCTAC would be GUAGAUC, which is same as base
Exp: ddNTPs (dideoxynucleotides) lack the 3’-OH
sequence of non-template strand except that all Ts
group required for the formation of phosphodiester
are replaced with U.
bonds, leading to termination of DNA polymerization
during Sanger sequencing by not allowing DNA Q. Although Apo B 48 and Apo B 100 are derived from
polymerase reaction. the same gene but are finally translated into separate
proteins. This is mainly due to ? (FMGE Jan 2023)
Q. DNA packing is done by? (NEET 2022)
A. DNA gene mutation in intestines
A. Histone
B. Point mutation in liver
B. Glycoprotein
C. DNA gene splicing
C. Nucleic acid
D. RNA editing
D. Helicases
E. Cytochromes Exp: The Apo B mRNA undergoes RNA editing in the
intestine, where a cytosine (C) is deaminated to uracil
Exp: DNA packing is primarily done by histones, which (U), resulting in the synthesis of Apo B48 protein
are proteins that form complexes with DNA to create instead of Apo B100.
a condensed structure called chromatin.

Q. When a codon is changed to stop codon, then it is: MISCELLANEOUS

(NEET 2022)
Respiratory QuotientQ
A. Stop codon mutation
B. Non-sense mutation Amount of CO2 Produced
C. Mis sense Mutation RQ =
Amount of O2 Utilized
D. Silent Mutation
RQ values
Exp: When a codon is changed to a stop codon, it
is referred to as a non-sense mutation, leading to •• Glucose (Carbohydrates) = 6/6 = 1
premature termination of protein synthesis.
•• Proteins = 0.8
Q. True about telomeres and telomerase is: (NEET •• Fats = 0.7
2022)
•• Mixed diet = 0.85
A. Increased telomere length with ageing
•• Alcohol = 0.66
B. Gradually decreasing length of telomeres with
ageing •• Excessive/High Carbohydrate diet > 1 (1.2).
C. Telomeres have coding sequences •• RQ decreases in Diabetes as RQ of fats is
D. Telomerase is found in somatic cells less than the RQ for carbohydrates, But on
giving Insulin, RQ again rises
Exp: Telomeres, the protective caps at the ends of
chromosomes, tend to shorten with each cell division RQ decreases in RQ increases in
and are associated with aging. •• Fasting •• Exercise
•• Starvation •• Fever
Q. The base sequence of the strand of DNA used as
•• Diabetes •• Acidosis
the template for transcription has the base sequence
GATCTAC. What is the base sequence of RNA •• Alkalosis
product? (INICET May 2023)
Collagen
A. CUAGAUG
•• Most abundant human protein
B. GTAGATC
•• 1° structure:
C. GTAGATC
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–– (Glycine - X - Y) n i.e. every 3rd amino acid is Copper (Cu) as cofactor, so Cu deficiency also
GlycineQ leads to decrease strength in collagen
–– X, Y can be Proline, Hydroxyproline, Lysine,
Plasma Proteins
Hydroxylysine
1. Transthyretin/ Pre-albumin
•• 28 types found in body
•• Used in transport of thyroxine & Retinol Binding
Important Collagen typesQ Protein (RBP)

Type Mnemonic Location

2. Ceruloplasmin

I S Skin (most abundant) •• Present in plasma and help in transport of Cu

II C Connective tissue •• It is synthesized in liver as apoceruloplasmin

(Apo Cp)
III A Arteries and CVS (healing and
granulation tissues) •• Apo cp binds 6 Cu atoms & forms active
IV B Basement membrane of Glomerulus ceruloplasmin (Cp)
VII Junction of dermis & epidermis •• So, it carries Cu from liver to peripheral
tissuesQ
Disease of collagen •• It also has Ferro-oxidase activity and converts
1. Alport Syndrome Fe+2 to Fe+3 which is required for iron transport
in body.
•• Collagen Type IV is defectiveQ
•• Clinical features are: Hematuria and End stage Menke and Wilson Disease
renal disease
Difference between Menke’s and Wilson’s
2. Epidermolysis bullosa Disease
•• Collagen Type VII is defectiveQ Menke’e Disease Wilson’s disease

•• Clinical features are skin blisters •• Cu Deficiency •• Cu Excess

•• ATP-7A protein •• ATP-7B protein defective
Post Translational Modifications (PTM) defective
of Collagen •• X-linked recessive •• Autosomal recessive

1. Hydroxylation of proline and lysine residues, to •• ATP-7A is present •• ATP-7B is present in liver
increase H-bonds in intestine for to throw Cu in bile and
absorption of Cu. Its also incorporates Cu in Cp.
deficiency causes: Its deficiency causes:
○○ ↓ Cu (Cu stays ○○ ↑ Cu in liver (due to
in intestinal cell, non-excretion from
unable to enter body)
blood) ○○ ↓ ceruloplasmin
○○ ↓ ceruloplasmin (Cp) (due to non-
(Cp) (due to incorporation of Cu in
insufficient Cu to Cp)
Clinical Significance: The deficiency of vitamin C will form Cp)
hinder these reactions resulting in fragile collagen of
blood vessels of gums which can be easily bruised and Note: ↓ Ceruloplasmin (Cp) is common between Menke
bleed during brushing causing scurvy. and Wilson Disease
1. Glycosylation Menke’s kinky hair syndrome- Clinical
•• Addition of carbohydrate in collagen which features
helps in making Aldol condensation
•• Premature birth
•• Enzyme required is Lysyl oxidase which require
•• Hypotonia
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•• Growth retardation
•• Mental retardation
•• Grey depigmented hair:
–– Tyrosinase (an oxidase) is affected as
oxidases require Cu
–– Tyrosinase is required for synthesis of
Melanin.
–– So, melanin synthesis is decreased causing
grey hair
•• Brittle kinky hair
–– As lysyl oxidase affected, so defective and
weak collagen synthesis
•• Decreased Cu in blood and urine

•• Treatment: Give penicillamine – as it will chelate

Cu

Vitamins
Water soluble Fat soluble
•• Vit B, vit C •• Vit A, D, E, K
•• Usually acts as •• Stored in body & don’t act
coenzyme & are not as coenzyme
Wilson’s hepatolenticular degeneration stored in body •• Exception: Fat soluble
•• Exception: One Vitamin which act as
Clinical features water-soluble vit coenzyme - Vit K
•• Cu accumulates in liver causing liver damage which get stored in
body - Vit B12
•• When excess in liver, ↑ Cu can go to other
extrahepatic tissues and cause following
changes: Important Information

–– In Brain – Neurological degeneration Q. Water Soluble form available for which fat-
soluble vitamin?
–– In Kidneys- Renal damage, urolithiasis
Ans: Vit K - Synthetic form – K3 /menadione is water
–– In Bone marrow & RBC - Hemolytic anemia
soluble
–– In Eyes -
→ Sunflower cataract
→ Kayser-Fleisher (KF) rings - green/golden
ring in Descemet’s membrane of cornea due
to Cu deposition
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One Liners WHO Vitamin A deficiency grading

Vitamin Deficiency Anemias Clinical Feature Grading

Night blindness XN
Microcytic hypochromic Megaloblastic anemia Conjunctival xerosis X1A
anemia
Bitot’s spots X1B
•• Vit C - help in •• Vit B9 - No neurological
absorption of Fe symptoms Corneal xerosis X2

•• Vitamin B6 - coenzyme •• Vit B12 -progressive Corneal ulcer covering less than 1/3 of the X3A
of heme synthesis enz peripheral neuropathy corneal surface
ALA synthase Corneal ulcer covering greater than 1/3 of X3B
the corneal surface
Important Information Corneal scarring XS

•• Raw eggs have protein called avidin, which Xerophthalmic fundus XF

tightly binds to biotin causing its deficiency
by not allowing its absorption. Important Information
Most sensitive screening for Vitamin A deficiency:
•• Biotin is required for carboxylases so it
Blood concentrations of retinol in plasma or serum, which
will affect gluconeogenic enzyme pyruvate
is the main circulating form of Vitamin A. This can assess
carboxylase causing hypoglycemia.Q
subclinical vitamin A deficiency.
Vitamin A
•• Active form: Retinol Vitamin A toxicity
•• Main C/F is raised Intracranial tension
resembling Brain Tumour aka Pseudo Tumour
Cerebri

Vitamin D

•• Active form: Calcitriol or 1,25 dihydroxy

cholecalciferol
–– Three -OH groups present at positions 1,3
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and 25 in cholesterol Vitamin K

Vitamin D deficiency Biochemical role: Blood clotting by activation of
clotting proteins 2 (II), 7 (VII), 9 (IX), and 10 (X) by
Deficiency in Children – RicketsQ carboxylation of their glutamate residues.Q
•• Beaded appearance of RIBs aka Rachitic Rosary
•• Hot cross bun appearance of head due to non-
closure of fontanelle
•• Bowlegs and Knock Knees
Deficiency in adults – Osteomalacia
•• Soft bones with frequent fracture
•• Waddling gait

Hypervitaminoses D
Symptoms
•• Hypercalcemia
•• Hypercalciuria causing Renal stones
•• Calcification of Soft tissues: calcium deposited Vit K deficiency
in blood vessels causing hypertension
•• Easy bruising
Vitamin E •• Bleeding tendencies
•• Most potent lipid phase antioxidant (chain •• ↑ Prothrombin time
breaking antioxidant)Q
•• Haemorrhagic disease of new-bornQ
•• Other antioxidant vitamins: Vit C, A and D
–– Fatal and occurs quite often, so, all new-borns
•• Vit E work synergistically with Se, Glutathione are given vit K injection
and Vit C for its antioxidant role
Important Information
C/F of Vit E Deficiency Reasons of Haemorrhagic disease of newborn
•• progressive peripheral neuropathy •• Intestine of a new-born is sterile (i.e. intestinal
bacteria for Vit K synthesis not present)
•• Hemolysis Q

•• Poor placental transfer

•• No megaloblastic anaemia
•• Low Vit K content in early breast milk (colostrum)
•• Opthalmoplegia •• Hepatic Immaturity - Inadequate synthesis of
coagulation proteins

Difference between Vit K and Vit C deficiency

Vit K deficiency Vitamin C deficiency
•• ↑ Prothrombin time •• ↑ Bleeding time
•• Associated with Fat malabsorption and Long-term •• Associated with dietary deficiency of citrus fruits and
antibiotic therapy fresh vegetables
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ONE LINERS
cGMP as second messenger inQ
•• Vitamin A visual cycle
•• NO induced vasodilation effects
•• Activation of ANP and BNP
Lipid deficiency causing retinitis pigmentosa: DHA (DocosaHexaenoic Acid)

Best method to determine HbA1c – Ion exchange chromatographyQ

Best Investigation for any inborn error of Metabolism (IEM) - Mass spectrometryQ

Buffer is most effective when its: pH = pKaQ

Maximum buffering zone of a buffer at: pH = pKa ± 1
Minimum buffering when pH = pI
Major extracellular buffer – Bicarbonate buffer
An ideal buffer as both components (HCO3- / CO2) can be altered for blood pH maintenance
Major intracellular buffer/urinary buffer – Phosphate buffer
Vitamin C cannot be formed in humans due to absence of enzyme: L-Gulono Lactone Oxidase
Vitamins synthesized by bacterial flora - Vitamins B2, B5, B7, and Vit KQ
Atypical vitamins – Vit that can be synthesized in our body by human enzymes e.g. Vitamin D and Niacin (B3)
Vitamins which is not present in vegetarian diet – Vitamin D & vitamin B12
Vitamin def with neurological symptoms – B1, B3, B6, B12 and Vit E.
Note: both B12 and E have peripheral Neuropathy but there is always megaloblastic anemia in B12 def whereas Vit E
def causes hemolysis
Site of absorption:
Vitamin B9 – Jejunum and duodenum
Vitamin B12 – Ileum (requires intrinsic factor def of which causes pernicious anemia)
Fructosamine (which is used for assessing long term glycemic control in a person with hemolysis) is a glycated product
of Albumin.
Alcohol is called Spurious liquor or Hooch, when the amount of methanol added is high enough that it can turn fatal
due to increased production of Formic acid, which leads to Metabolic acidosis, blurred vision, blindness, neurological
damage, respiratory failure & death. This was the reason for Hooch Tragedy.
•• Two B-complex vitamins which causes toxicity are:
1. B3 (Flushing, nausea, vomiting, glucose intolerance, hyperuricemia, hepatic toxicity, macular edema & cysts)
2. B6 (sensory neuropathy)
•• DASH diet - Dietary Approach to Stop Hypertension
○○ Poor in Na
○○ Increased K, Ca, Mg (Fruits, whole grains & Vegetables)

PREVIOUS YEAR’S QUESTION Exp: Type I collagen is the most abundant collagen
type in the human body, including the skin. It provides
Q. Type of collagen Maximum in skin? (NEET Jan structural support and tensile strength to the skin
2019)
Q. Defect in Menke disease? (NEET Jan 2019)
A. Type I
A. Lysyl hydroxylase
B. Type II
B. Lysyl oxidase
C. Type III
C. Prolyl hydroxylase
D. Type IV
D. Prolyl oxidase
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Biochemistry

Exp: Menke disease is a genetic disorder characterized D. 1.25

by impaired copper absorption leading to def of Cu
Exp: Respiratory quotient (RQ) is the ratio of
which is a cofactor for enzyme lysyl oxidase. So,
carbon dioxide produced to oxygen consumed during
a decreased activity of this enzyme is seen in this
metabolism. RQ is calculated by dividing the volume of
disease.
CO2 produced (200 ml) by the volume of O2 consumed
Q. Most potent lipid phase antioxidant? (FMGE June (250 ml), resulting in an RQ of 0.8.
2019)
Q. Which factor in warfarin therapy, have decreased
A. Vitamin A gamma carboxylation of glutamate residue? (NEET
B. Vitamin E Jan 2020)
C. Vitamin C A. Factor II
D. Vitamin K B. Factor V
Exp: Vitamin E is a potent antioxidant that protects C. Factor VIII
cell membranes from oxidative damage by lipid D. Factor III
peroxidation. It scavenges free radicals in the
Exp: Warfarin inhibits the enzyme vitamin K epoxide
lipid phase, preventing the propagation of oxidative
reductase (VKOR), which is responsible for the
reactions.
conversion of vitamin K epoxide to its reduced form,
Q. Alcoholic patient with neurological Symptoms, vitamin K hydroquinone. This reduced form is required
there is deficiency of which Vitamin? (FMGE Aug for the gamma carboxylation of glutamate residues in
2020) coagulation factors, including Factor II (prothrombin).

A. B1 Q. Vitamin D synthesis sequence is? AIIMS June 2020)

B. A A. Skin → liver → kidney
C. B9 B. Kidney → Live → Skin
D. B12 C. Skin → kidneys → liver
Exp: Chronic alcohol consumption can lead to thiamine D. Live → Skin → kidney
deficiency, which can manifest as neurological
Exp: Vitamin D synthesis begins in the skin, where
symptoms such as Wernicke-Korsakoff syndrome.
sunlight converts 7-dehydrocholesterol to previtamin
Thiamine is essential for normal brain function and
D3. Previtamin D3 is then converted to vitamin D3
energy metabolism.
in the liver. Finally, in the kidneys, vitamin D3 is
Q. Vitamin deficiency related to neonatal seizures? converted to its active form, calcitriol.
(AIIMS June 2020)
Q. Methyl tetrahydrofolate accumulation and
A. Thiamine functional deficiency of folate is seen in the deficiency
B. Pyridoxine of: (INICET 2021)
C. Riboflavin A. Folic acid
D. Pantothenic Acid B. Vit B12
Exp: Neonatal seizures can be associated with C. Vit B1
pyridoxine (Vitamin B6) deficiency. Pyridoxine is D. Vit B6
required for the synthesis of neurotransmitters and
Exp: Methyl tetrahydrofolate is the active form of
proper functioning of the nervous system.
folate, and its accumulation occurs in vitamin B12
Q. A person of 50 kg weight, his CO2 & O2 levels deficiency. Vitamin B12 is required for the conversion
were measured from spirometry as CO2 = 200 ml, O2 of methyl tetrahydrofolate to tetrahydrofolate.
= 250 ml. What is RQ in this case? (INI CET Nov
Q. Which of the following supplement is required
2020)
more for a lactating woman than the pregnant female?
A. 4 (INICET 2021)
B. 5 A. Vit A
C. 0.8
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B. B12 4. Albumin - b. Free fatty acids

C. Calcium
Q. Fructosamine (which is used for assessing long
D. Thiamine term glycemic control in a person with hemolysis) is a
Exp: Lactation increases the demand for various glycated product of: (INICET Nov 2022)
nutrients, including vitamin A. Therefore, a lactating A. Glycosaminoglycan
woman requires a higher amount of vitamin A compared
B. Urea
to a pregnant female.
C. Fructose
Q. Sideroblastic anemia can be treated by? (INICET D. Albumin
July 2021)
Exp: Fructosamine is a glycated product formed
A. Pyridoxine by the non-enzymatic glycation of serum proteins,
B. B1 primarily albumin. It is used to assess long-term
C. B3 glycemic control in individuals with conditions such as
hemolysis that can interfere with traditional glycated
D. B12
hemoglobin (HbA1c) measurements
Exp: Sideroblastic anemia is a group of blood
disorders characterized by impaired iron utilization Q. Hooch tragedy is related to which of the following
in the production of hemoglobin. Pyridoxine (Vitamin alcohols? (INICET Nov 2022)
B6) supplementation can improve the condition, as it A. Methyl alcohol
is involved in heme synthesis.
B. Ethyl alcohol
Q. Uracil was found in genetic code. Which vitamin C. Ethylene glycol
deficiency leads to this condition: (INICET May 2022) D. Hyporglycin
A. B12 Exp: The term “hooch tragedy” refers to incidents
B. B6 involving the consumption of illicitly produced or
C. Folate contaminated alcohol. Methanol (methyl alcohol)
is commonly associated with such tragedies, as its
D. Vit E consumption can lead to severe toxicity and even death.
Exp: Uracil is converted to thymine by enzyme
Q. A woman on anti-depressants presents with bleeding.
thymidylate synthase by methylation where methyl
She gives a history of bulky stools which sticks to the
group is donated by methyl-THF. So, a deficiency
pan. Which of the following vitamin deficiency can
Folate will result in thymine deficiency and may lead
cause bleeding in this condition? (NEET 2022)
to uracil appearing in the DNA in place of thymine.
A. Vitamin A
Q. Match the following transporters with the
B. Vitamin D
molecule they carry. (INICET May 2022)
C. Vitamin E
1. Hemopexin a. Thyroxin D. Vitamin K
2. Haptoglobin b. Free fatty acids
Exp: Vitamin K deficiency can lead to impaired blood
3. Pre-albumin c. Heme clotting and bleeding tendencies. Bulky stools that
4. Albumin d. Haemoglobin stick to the pan may indicate malabsorption, which can
affect the absorption of fat-soluble vitamins such as
A. 1b, 2a, 3c, 4d vitamin K.
B. 1a , 2c, 3b, 4d Q. Condition shown below is due to which vitamin
C. 1c, 2a, 3d, 4b deficiency? (NEET 2022)
D. 1c, 2d, 3a, 4b

Exp: 1. Hemopexin - c. Heme

2. Haptoglobin - d. Haemoglobin
3. Pre-albumin - a. Thyroxin A. Vitamin A
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Biochemistry

B. Vitamin B Exp: Scurvy is characterized by defective collagen

C. Vitamin C synthesis due to the deficiency of vitamin C, which is
required for the hydroxylation of proline and lysine
D. Vitamin K
residues in collagen synthesis
Exp: The condition shown in the image appears to
be Bitot’s spot (superficial deposition of keratin Q. A patient was presented to OPD with features of
in conjunctiva) which occur in case of vitamin A collagen vascular disorder. Which of the following
deficiency. deficits is most likely to be associated with defective
collagen formation? (FMGE Jan 2023)
Q. Diarrhea, dementia and dermatitis is caused by
A. Ascorbic acid
deficiency of (NEET 2023)
B. Copper and Iron
A. Biotin
C. Both A & B
B. Niacin
D. Zinc & Magnesium
C. Thiamine
Exp: Post translational modification of collagen on
D. Riboflavin
proline and lysine residue is required for its proper
Exp: Diarrhea, dementia, and dermatitis are classic hydrogen bond formation and crosslinking which
symptoms of pellagra, which is caused by niacin provide strength to collagen fibers. These reactions
(vitamin B3) deficiency. Niacin is important for energy require vitamin C, copper and iron as cofactors for
production and metabolism and deficiency can lead to the enzyme involved in these processes.
various systemic symptoms
Q. Xerophthalmia/ conjunctival xerosis occurs due to
Q. Chronic alcoholic with features of ataxia confusion deficiency of which of the following vitamin: (FMGE
and 6th nerve involvement? Most commonly seen in Jan 2023)
deficiency of? NEET 2023)
A. Vitamin B1
A. Thiamine B. Vitamin B3  
B. Riboflavin C. Vitamin A
C. Niacin D. Vitamin D
D. Cobalamin
Exp: Xerophthalmia and conjunctival xerosis are
Exp: Alcohol impairs thiamine absorption and ocular manifestations of vitamin A deficiency, which
increases its excretion, leading to thiamine deficiency can lead to dryness, night blindness, and eventually
and neurological symptoms. blindness.
Q. Baby with h/o raw egg ingestion. (picture of baby’s
scalp hairloss) deficiency of which vitamin? (NEET
2023)
A. Biotin
B. Thiamine
C. Riboflavin
D. Pyridoxine
Exp: Raw egg white contains avidin, which binds to
biotin and prevents its absorption, leading to biotin
deficiency and hair loss.

Q. The biochemical basis of scurvy is? (NEET 2023)

A. Impaired collagen synthesis
B. Increased keratinization of epithelium
C. Inhibition of clotting factors
D. Low calcium