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Bio Ch5

The document outlines the mechanisms of hormone action within the endocrine system, detailing the classification of hormones by chemical structure (peptides, steroids, and amino acid derivatives) and their effects on target tissues. It explains the roles of the hypothalamus and pituitary gland in regulating hormone release, including the interactions between the anterior and posterior pituitary. Additionally, it covers the functions of thyroid hormones and calcitonin in metabolic regulation and calcium homeostasis.

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0% found this document useful (0 votes)
11 views46 pages

Bio Ch5

The document outlines the mechanisms of hormone action within the endocrine system, detailing the classification of hormones by chemical structure (peptides, steroids, and amino acid derivatives) and their effects on target tissues. It explains the roles of the hypothalamus and pituitary gland in regulating hormone release, including the interactions between the anterior and posterior pituitary. Additionally, it covers the functions of thyroid hormones and calcitonin in metabolic regulation and calcium homeostasis.

Uploaded by

zhiqingguo15
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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5.

1 Mechanisms of Hormone Action


1. The endocrine system consists of organs called glands, which secrete hormones into the
bloodstream that bind to distant receptors.

Classification of Hormones by Chemical Structure


1. By chemical identities, hormones can be peptides, steroids, or amino acid derivatives.

Peptide Hormones

1. Peptide hormones are made up of amino acids.


2. Peptide hormones range in size from quite small (e.g. anti-diuretic hormone, ADH) to
relatively large (e.g. insulin).
3. Peptide hormones are all derived from larger precursor polypeptides that are cleaved
during posttranslational modification. They are then modified in the Golgi apparatus and
transported out in vesicles.
4. Peptide hormones cannot pass through the plasma membrane because they are charged.
They bind to extracellular receptors as first messengers and trigger second messengers.
This is known as a signaling cascade.
1. At each step of the signaling cascade, there is a possibility of amplification. (e.g.
one hormone molecule binds to multiple receptors before it is degraded. / Each
receptor activate multiple enzymes, which trigger more second messengers.)
2. Common second messengers: cyclic adenosine monophosphate (cAMP),
inositol triphosphate (IP3), Ca2+.
5. Extracellular receptors have many different subtypes, each with different mechanisms.
6. G-protein-coupled receptors include the following common pathways:
1. cAMP pathway: A G protein-coupled receptor can trigger or inhibit an enzyme
called adenylate cyclase, raising or lowering the levels of cAMP
accordingly(turn ATP into cAMP). cAMP can bind to intercellular targets such as
protein kinase A, which phosphorylate transcription factors like cAMP response
element-binding protein
(CREB).

2. Phospholipase C(PLC) pathway:


1. The G protein heterotrimer (alpha, beta, gamma subunits) attaches to the
intracellular portion of the GPCR, a transmembrane cell surface receptor.
When the ligand binds to the extracellular domain of the receptor, the
GDP molecule initially bound to the G protein alpha subunit is released,
and a GTP molecule binds the G protein in its place.
2. The GTP-bound alpha subunit dissociates from the beta and gamma
subunits and activates the membrane-bound enzyme phospholipase C
(PLC).
3. PLC hydrolyzes the membrane phospholipid phosphatidylinositol
bisphosphate (PIP2) into inositol trisphosphate (IP3) and diacylglycerol
(DAG).
4. Water-soluble IP3 diffuses from the cell membrane through the cytoplasm
to bind IP3 receptors located on the endoplasmic reticulum and
mitochondria. Binding of the IP3 receptor opens calcium channels,
allowing the release of stored calcium into the cytoplasm, which activates
protein kinase C (PKC).
5. DAG diffuses within the membrane and activates PKC.
6. PKC phosphorylates downstream intracellular proteins to produce its
physiologic effects.

 Protein kinase A can phosphorylate other enzymes or transcription factors, therefore it


can have a rapid or slow effect on the cell.
 The effects of peptide hormones are rapid but short-lived. Easy turn on and off. Needs
constant stimulation to last.
 Peptides are usually water-soluble, so peptide hormones usually travel in the bloodstream
without carriers.

Steroid Hormones

1. Derived from cholesterol, produced primarily by the gonads and adrenal cortex. E.g.
estrogen.
2. Nonpolar, can easily cross the cell membrane. Thus, their receptors are usually
intracellular or intranuclear.
3. Upon binding to the receptor, the steroid hormone-receptor complex undergoes
conformational changes such as dimerization. The receptor binds to the DNA and
interferes with transcription.
4. The effects of steroid hormones are slower but longer-lived because DNA is directly
altered causing alterations in the amount of mRNA and protein.
5. Steroid hormones are not water-soluble so they need carrier proteins to travel in the
bloodstream.
1. Some carrier proteins are specific(e.g. sex hormone-binding globulin) and some
are nonspecific (e.g. albumin).
2. Hormones are generally inactive while attached to a carrier protein. So the levels
of carrier protein can change the levels of active hormone. The more carrier
protein there is, the less active hormone is at work.
Amino Acid-Derivative Hormones

1. Amino acid-derivative hormones are derived from one or two amino acids(either
tyrosine or tryptophan), usually with a few additional modifications.
2. Common examples: epinephrine, norepinephrine, triiodothyronine, and thyroxine.
(Includes catecholamines and thyroid hormones).
3. E.g. thyroid hormones are made from tyrosine modified by the addition of several iodine
atoms.
4. The chemistry of this family is less predictable, remember:
1. catecholamines (epinephrine, norepinephrine) bind to G protein-coupled
receptors.
2. thyroid hormones bind intercellularly.
5. Note that most peptide and amino acid-derivative hormones have names that end in -in,
or -ine (insulin, vasopressin, thyroxine, triiodothyronine...). Most steroid hormones have
names that end in -one, -ol, or -oid (testosterone, aldosterone...).

Classification of Hormones by Target Tissue


1. Direct hormones: secreted and act directly on the target tissue. E.g. insulin by pancreas.
2. Tropic hormone: stimulates the production of another hormone by another endocrine
gland that acts on the target tissues. E.g. GnRH, LH.
3. Some hormones act both as direct and tropic hormones.
5.2 Endocrine Organs and
Hormones

Hypothalamus
1. The hypothalamus is the bridge between the nervous and endocrine systems.
2. The hypothalamus regulates the pituitary gland through tropic hormones. It is located in
the forebrain, directly above the pituitary gland and below the thalamus.
3. The hypothalamus and the pituitary are close together, they use paracrine release of
hormones into a portal system that directly connects the two organs.
4. The hypothalamus receives input from a wide variety of sources.
5. The release of hormones by the hypothalamus is regulated by negative feedback.
6. The pituitary gland has an anterior and posterior component, each has a unique
interaction with the hypothalamus.
1. The two pituitary lobes are both derived from embryonic ectodermal tissue but
differ in composition. The anterior pituitary is derived from epithelial cells from
the developing roof of the mouth and contains typical glandular endocrine cells,
whereas the posterior pituitary is derived from ectodermal neural tissue in the
developing brain and does not contain typical glandular endocrine cells.

Interactions with the Anterior Pituitary

1. A blood vessel system called the hypophyseal portal system directly connects the
hypothalamus with the anterior pituitary. Hormones released by the hypothalamus travel
to the pituitary and cannot be found in appreciable concentrations in the systemic
circulation. They travel down the pituitary stalk and bind to receptors in the anterior
pituitary.
2. Common hormones involved:
1. Gonadotropin-releasing hormone (GnRH) --- follicle-stimulating hormone (FSH)
and luteinizing hormone (LH)
2. Growth hormone-releasing hormone (GHRH) --- growth hormone (GH)
3. Thyroid-releasing hormone (TRH) -- thyroid-stimulating hormone (TSH)
4. Corticotropin-releasing hormone (CRH) --- adrenocorticotropic hormone (ACTH)
5. An exception: prolactin-inhibiting factor (PIF), actually dopamine --- causes a
decrease in prolactin. A tumor in the pituitary may suppress the portal system.
More prolactin will be released, causing milk production in a male or nonpregnant
female.
3. Three organ systems are commonly referred to as axes. E.g. the hypothalamic-pituitary-
adrenal (HPA) axis. / the hypothalamic-pituitary-ovarian (HPO) axis.

Interactions with the Posterior Pituitary

1. The posterior pituitary does not receive tropic hormones through the hypophyseal portal
system. Rather, neurons in the hypothalamus send their axons down the pituitary stalk
directly into the posterior pituitary, which can then release oxytocin and antidiuretic
hormones.
2. The posterior pituitary is a storage site for neurohormones (ie, hormones released from
neurons rather than from typical glandular endocrine cells) produced by hypothalamic
neurons whose axons extend down into the posterior pituitary. When stimulated, these
neurohormones are released by exocytosis from the axons into the small blood vessels
that carry blood away from the posterior pituitary.

3. Oxytocin: stimulates uterine contraction during labor, milk letdown during lactation, and
bonding behavior.
4. Antidiuretic hormone (ADH, also called vasopressin): increases reabsorption of water
in the collecting ducts of the kidneys. Secreted in response to increased plasma
osmolarity and increased concentration of solutes in blood.

Anterior Pituitary
1. The anterior pituitary synthesizes and secretes seven different products. Four are tropic
hormones, three are direct hormones.
2. FLAT PEG

Hormones synthesized & secreted by the anterior pituitary gland


Hormone Secretion stimulated Action
by
o Ovaries: stimulates follicle
Gonadotropin- maturation
Follicle-stimulating
releasing hormone o Testes: stimulates
hormone (FSH)
(GnRH) spermatogenesis

o Ovaries: stimulates production


of estrogen & triggers
Luteinizing hormone ovulation
GnRH
(LH) o Testes: promotes synthesis of
testosterone

o Targets adrenal cortex to


Corticotropin-
Adrenocorticotropic promote release of
releasing hormone
hormone (ACTH) glucocorticoids
(CRH)
Thyrotropin- o Causes thyroid to release
Thyroid-stimulating
releasing hormone thyroid hormones (T3 & T4)
hormone (TSH)
(TRH)
o Targets a variety of tissues (eg,
Growth hormone– muscle, bone, liver) to promote
Growth hormone (GH) releasing hormone cellular growth & degradation
(GHRH) of fats

o Target opiate receptors in the


brain to diminish pain
β-Endorphins CRH
perception

Decreased prolactin-
o Stimulates lactation
Prolactin inhibiting hormone
(PIH)

Tropic Hormones

1. Follicle-stimulating hormone (FSH)


2. Luteinizing hormone (LH)
3. Adrenocorticotropic hormone (ACTH)
4. Thyroid-stimulating hormone (TSH)

Direct Hormones

1. Prolactin: stimulates milk production in the mammary glands. During pregnancy, the
high levels of estrogen and progesterone allow for the development of milk ducts, but it is
not until shortly after the expulsion of the placenta, when estrogen, progesterone, and
dopamine levels drop, that the block on milk production is removed and lactation begins.
o When the infant latches on to the breast, nipple stimulation causes activation of
the hypothalamus, leading to: (1) oxytocin results in contraction of the smooth
muscle of the breast. (2) stop releasing dopamine, which allows prolactin release.
2. Endorphins decrease the perception of pain. Morphin mimics the effect of this naturally
occurring painkiller.
3. Growth hormone (GH): promotes the growth of bone and muscle.
o This is energetically expensive and requires large quantities of glucose. Growth
hormone prevents glucose uptake in tissues that are not growing and stimulates
the breakdown of fatty acids(not protein!!), which increases the availability of
glucose overall.
o GH is an anabolic hormone, which means it exerts a positive effect on protein
synthesis and cell growth in numerous tissues. (anabolic 合成代谢,catabolic 分解代谢).
o Bone growth originates in epiphyseal plates that seal shut during puberty. An
excess of GH in childhood causes gigantism, and a deficit results in dwarfism.
For adults, an excess of GH causes acromegaly. The long bones are seals, so GH
generally affects the small bonds in the bands, feet, and head.

Posterior Pituitary
1. The posterior pituitary contains nerve terminals of neurons with cell bodies in the
hypothalamus. It receives and stores ADH and oxytocin. The posterior pituitary does not
synthesize any hormones itself.

Hormones secreted by the posterior pituitary


Secretion stimulated
Hormone Action
by
o Uterus: Promotion of contractions
Oxytocin Nerve impulses o Mammary glands: Milk ejection

o Promotion of water reabsorption by the


Vasopressin Nerve impulses kidneys

2. ADH:

1. secreted in response to low blood volume (sensed by baroreceptors), and


increased blood osmolarity (sensed by osmoreceptors).

2. Acts on collecting ducts on the nephron. The permeability of renal collecting


ducts is increased, and water is reabsorbed passively.
3. Oxytocin:
1. secreted during childbirth.
2. Allows for coordinated contraction of uterine smooth muscle, smooth muscle in
the breast, and bonding behavior.
3. Positive feedback loop. Have a definitive endpoint--in this case, delivery.
Thyroid
1. Thyroid is located on the front surface of the trachea. Controlled by thyroid-stimulating
hormone from the anterior pituitary.
2. Functions:
1. Setting basal metabolic rate by releasing triiodothyronine (T3).
2. Promote calcium homeostasis by releasing calcitonin.

Triiodothyronine and Thyroxine

1. Triiodothyronine (T3) and thyroxine (T4) are both produced by the iodination (of 3 and
4 iodine atoms respectively) of the amino acid tyrosine in the follicular cells of the
thyroid.

2. They reset the basal metabolic rate of the body by making energy production more or less
efficient, as well as altering the utilization of glucose and fatty acids. Increased amounts
of T3 and T4 lead to increased cellular respiration, thus increasing protein and fatty acid
turnover. They induce bone resorption too.
3. Negative feedback with TSH and TRH.
4. A deficiency of iodine or inflammation of the thyroid may result in hypothyroidism,
meaning an insufficient amount of thyroid hormones.
1. Effects: lethargy, decreased body temperature, slowed respiratory and heart rate,
cold intolerance, and weight gain.
2. Thyroid hormones are required for neurological and physical development in
children. Children with hypothyroidism may experience intellectual disability and
developmental delay (cretinism).
5. An excess of thyroid hormones, which may result from a tumor or thyroid over-
stimulation, is called hyperthyroidism.
1. Effect: heightened activity level, increased body temperature, increased
respiratory and heart rate, heat intolerance, and weight loss.
Calcitonin(降血钙素)

1. There are two distinct cell populations in the thyroid gland.


1. Follicular cells produce thyroid hormones.
2. C-cells (also called parafollicular cells) produce calcitonin.
2. Function of calcitonin: decreases plasma calcium levels. Stimulated by high levels of
calcium in the blood.
3. Mechanisms:
1. Increase calcium excretion from the kidney.
2. Decrease calcium absorption from the gut.
3. Increase the storage of calcium in the bone. (decrease osteoclast activity)
4. Calcium is important for the body with the following critical roles:
1. Bone structure and strength.
2. Release of neurotransmitters from neurons.
3. Regulation of muscle contraction.
4. Clotting of blood. (Calcium is a cofactor).
5. Also plays a role in cell movement and exocytosis of cellular materials.
Parathyroid Glands
1. Parathyroids are four small pea-sized structures on the posterior surface of the thyroid.

2. The hormone they release is called parathyroid hormone (PTH).


3. PTH is antagonistic to calcitonin, raising blood calcium levels.
4. Mechanism:
1. Decrease calcium excretion from the kidney.
2. Increase calcium absorption from the gut (via vitamin D).
3. Increase bone resorption by osteoclasts, thereby freeing up calcium and
decreasing bone mineralization. The majority of calcium in the body is stored as
hydroxyapatite [Ca10(PO4)6(OH)2], a mineral found in the bone matrix that
primarily contributes to bone strength and hardness. Osteoclast-mediated bone
destruction (ie, resorption) causes the calcium stored in the matrix to be released
into the blood, dissolving mineralized bone and increasing plasma calcium levels.

5. Subject to feedback inhibition.


6. PTH also promotes phosphorus homeostasis by increasing the resorption of phosphate
from bone and reducing the reabsorption of phosphate in the kidney.
7. PTH also activates vitamin D, which is required for the absorption of calcium and
phosphate in the gut.

o PTH increases the activity of the enzyme that catalyzes the final step in the
conversion of inactive circulating vitamin D into its active form, calcitriol.
Vitamin D can be absorbed from dietary sources or produced from its cholesterol
precursor in a process requiring skin exposure to ultraviolet light. However,
successive reactions must occur for vitamin D to become physiologically active.
The first reaction occurs in the liver and the second, which is stimulated by PTH,
occurs in the kidneys to create active 1,25-dihydroxyvitamin D (calcitriol).

8. Overall effect of PTH:


1. Increase in blood calcium levels.
2. Little effect on phosphate (the absorption of phosphate in the gut and its excretion
in the kidney somewhat cancel each other).

Adrenal Cortex
1. Adrenal glands are on top of the kidneys. Each adrenal gland consists of a cortex and a
medulla, each secretes different hormones.
2. The adrenal cortex secretes corticosteroids. It can be divided into three functional
classes: glucocorticoids, mineralocorticoids, and cortical sex hormones.

Glucocorticoids

1. Glucocorticoids are steroid hormones that regulate glucose levels. It also affects protein
metabolism.
2. Common examples: cortisol, cortisone.
1. They increase blood glucose by increasing gluconeogenesis and decreasing
protein synthesis.
2. They decrease inflammation.
3. Cortisol is a stress hormone, released in times of stress. Increase blood sugar as a
ready source of fuel.
3. Hypothalamic-pituitary-adrenal pathway (HPA axis): Corticotropin-releasing factor
(from the hypothalamus) --- adrenocorticotropic hormone (from anterior pituitary) ---
glucocorticoids (from the adrenal cortex).
4. Used in joint pain to decrease inflammation, and used to treat systemic inflammation
caused by allergic reactions or autoimmune disease.

Corticosteroid hormones secreted by the adrenal cortex


o Glucocorticoids (eg, cortisol): Increase energy availability by stimulating
lipolysis & gluconeogenesis (synthesis of glucose from noncarbohydrate sources
such as amino acids); also, have anti-inflammatory effects
o Mineralocorticoids (eg, aldosterone): Affect salt & water homeostasis in the
kidneys by promoting sodium reabsorption & excretion of potassium

Mineralocorticoids

1. Mineralocorticoids are used in salt and water homeostasis.


2. Common example: aldosterone. It increases sodium reabsorption in the distal convoluted
tubule and collecting duct of the nephron. Water follows the sodium cation, increasing
blood volume and pressure. Note that the plasma osmolarity is unchanged since water
and sodium flow together, this is in contrast to ADH, which only increases water
reabsorption. It also reduces reabsorption of potassium and hydrogen ions.
3. Under the control of the renin-angiotensin-aldosterone system.
1. Decreased blood pressure causes the juxtaglomerular cells of the kidney to
secrete renin.
2. Renin cleaves an inactive plasma protein, angiotensinogen, to its active
form, angiotensin I.
3. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme
(ACE) in the lungs.
4. Angiotensin II stimulates the adrenal cortex to release aldosterone.
4. Angiotensin II can also lead to vasoconstriction and an increase in heart rate. ACE
inhibitors are used to treat high blood pressure and congestive heart failure. Their names
end with -pril. The secretion of renin overall causes vasoconstriction.

Cortical Sex Hormones

1. The adrenal glands also make cortical sex hormones (androgens and estrogens).
2. Adrenal testosterone plays a small role in males because the testes already secrete a large
quantity. But ovaries secrete far smaller amounts of androgen, females are much more
sensitive to disorders of cortical sex hormone production.
3. An excess of androgen production causes no obvious phenotypic effects in a male fetus,
but for female fetus, may be born with ambiguous or masculinized genitalia. Males can
be affected by similar disorders if they lead to excessive production of estrogen.
4. In females, exposure to excess testosterone before birth would lead to abnormal
development of the female external genitalia that can be detected upon physical
examination at birth. Because testosterone is a normal contributor to male sexual
development, excess testosterone would not alter development of the external sex
organs as dramatically in males, and physical examinations during early infancy might
yield no abnormal results. High testosterone levels lead to abnormal sexual
development earlier in females than in males.

Adrenal Medulla
1. Responsible for the production of the sympathetic hormones
epinephrine and norepinephrine. They are secreted directly into the bloodstream by
specialized nerve cells(derived from ectoderm).
2. Although most tissues are innervated by both sympathetic and parasympathetic motor
fibers, the adrenal medulla is unique in that it is innervated only by the sympathetic
nervous system.
3. Epinephrine and norepinephrine are both amino acid-derivative hormones that belong to
a larger class of molecules known as catecholamines. Their chemical characteristics
are similar to peptide hormones.
4. Functions:
1. Redirection of blood flow through the body via vasoconstriction and vasodilation.
2. Increased heart rate and cardiac muscle contractility.
3. Dilation of airways.
4. Increases the breakdown of glycogen into glucose (glycogenolysis) in the liver
and muscle, increasing basal metabolic rate. Stress response.
5. Note that adrenal hormones do not affect the reabsorption of glucose in the
kidneys!
5. Both cortisol and epinephrine are involved in stress response. Cortisol is for long-term
(slow) stress responses. Epinephrine is for short-term (fast) stress responses. Cortisol
increases the synthesis of catecholamines.
Pancreas
1. The pancreas has both exocrine and endocrine functions.
1. Glands whose secretions are released onto an "exterior" body surface (such as the
skin or the inner surface of the lung) are called exocrine glands. Glands are
secretary cells grouped together. Some secretary cells form hollow tubes called
ducts into which their secretions flow.

2. Other secretory epithelial cells develop around blood vessels but lack ducts; these
cells release their secretions, called hormones, into the blood. Glands composed
of cells such as these are called endocrine glands.

3. Both endocrine and exocrine cells are epithelial cells that produce substances
released into the extracellular space. Exocrine secretions are released to the
body's "exterior," such as the skin or the inner surface of the gut or lungs.
Endocrine secretions are released into the blood.
2. Exocrine function: secrete digestive enzymes into pancreatic ducts, which fuse with the
bile duct into the duodenum 十二指肠.
3.

4. Endocrine function: It has small clusters of hormone-producing cells that are grouped
into islets of Langerhans. Islets secrete hormones into blood vessels. Islets contain three
types of cells, each secreting a different hormone:
1. alpha cells: glucagon
2. beta cells: insulin
3. delta cells: somatostatin

Glucagon

1. Glucagon is secreted when glucose levels are low. Triggered by low blood glucose or by
certain gastrointestinal hormones. Secreted by alpha cells.
2. Increases glucose production by triggering glycogenolysis, gluconeogenesis, and the
degradation of protein and fat.

Insulin

1. Insulin is antagonistic to glucagon, secreted when blood glucose is high.


2. Induces muscle and liver cells to take up glucose and store it as glycogen. Stimulates fat
and protein synthesis.
3. An excess of insulin leads to hypoglycemia, characterized by low blood glucose
concentration.
4. Underproduction, insufficient secretion, or insensitivity to insulin all can result
in diabetes mellitus, clinically characterized by hyperglycemia.
1. Presence of glucose in the urine: the ability of the nephrons to reabsorb glucose is
overwhelmed.
2. Polyuria 多尿 and polydipsia 烦渴.
5. Two types of diabetes mellitus:
1. Type I: insulin-dependent, caused by autoimmune destruction of the beta-cells of
the pancreas, resulting in low or absent insulin production. Require regular
injections of insulin.
2. Type II: non-insulin-dependent, result of receptor-level resistance to the effects
of insulin. Partially inherited and partially due to environmental factors, such as
high-carbohydrate diets and obesity.
6. Glucagon, growth hormone, glucocorticoids, and epinephrine are also capable of
increasing plasma glucose. They are commonly called counterregulatory hormones.
Somatostatin

1. Secreted by hypothalamus. Functions include:


1. Decreases growth hormone secretion.
2. Inhibit both insulin and glucagon secretion.
2. Somatostatin is produced in several locations in the body, including the hypothalamus
and pancreas.

Gonads
1. The testes and ovaries secrete testosterone and estrogen&progesterone respectively in
response to stimulation by gonadotropins (LH and FSH).
2. They are related to sexual differentiation during gestation and the development and
maintenance of secondary sex characteristics.

Pineal Gland
1. The pineal gland secretes the hormone melatonin, which is involved in circadian
rhythms. The precise mechanism is unclear.
2. Melatonin, a hormone that promotes drowsiness and sleep, is released by the pineal gland
in response to low light levels (detected by the
retina).

Other Organs
1. The kidney plays a role in water balance by ADH and renin-angiotensin-aldosterone
system. It also produces erythropoietin 红细胞生成素, which stimulates the bone marrow to
increase production of erythrocytes when blood oxygen levels are low.
2. The atria cells release atrial natriuretic peptide (ANP) to help regulate salt and water
balance.
1. It is secreted when the atria cells are stretches from excess blood volume.
2. It promotes the excretion of sodium and therefore increases urine volume.
3. It is antagonistic to aldosterone because it lowers blood volume and pressure with
no effect on blood osmolarity.
3. The thymus 胸腺 releases thymosin. It is important for proper T-cell development and
differentiation. The thymus is a lymphoid structure that is the site of T lymphocyte
maturation. T cell synthesis begins in the bone marrow but is not completed until
lymphoid progenitor cells (T cell precursors) migrate to the thymus, where they mature.
After this, the naïve T lymphocytes are released into circulation and are involved in cell-
mediated immunity. Thymus atropies by adulthood and thymosin levels drop
accordingly.
4. Endocrine tissue can be found in the gastrointestinal tract. They are often released in the
presence of specific nutrients.
1. Ghrelin is a hormone released by cells in the stomach (ie, part of the gut). In a
healthy individual, ghrelin is transported via the bloodstream to the brain, where it
acts on the hypothalamus to stimulate appetite.

2. Cholecystokinin is a gut-derived hormone that promotes satiety.


5. Leptin is a satiety hormone secreted by adipose tissue and acts on the hypothalamus. It
notifies the brain about the amount of fat stored in the body's fat cells. Secreted after a
meal(energy-rich state). The greater the adipose tissue stores, the higher leptin levels in
the serum.

Practise
1. Agonist 激动剂: An agonist is a chemical that activates a receptor to produce a biological
response. Receptors are cellular proteins whose activation causes the cell to modify what
it is currently doing.

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