5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

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Overview of the development of the

gastrointestinal tract
Author: All topics are updated as new evidence
Ian R Sanderson, MD becomes available and our peer review
Section Editor: process is complete.
Melvin B Heyman, MD, MPH Literature review current through: Apr
Deputy Editor: 2025.
Alison G Hoppin, MD This topic last updated: Aug 07, 2024.

INTRODUCTION
The anatomic formation of the esophagus, stomach, intestine, liver, and pancreas are
achieved in the fourth fetal week through a series of evaginations, elongations, and
dilatations. Anatomic development progresses through cell proliferation, growth, and
morphogenesis.

CEPHALOCAUDAD DIFFERENTIATION
Three distinct regions of the intestine give rise to specific portions of the
gastrointestinal (GI) tract:
●The foregut is the precursor of the pharynx, esophagus, stomach, liver, gall bladder,
pancreas, and the cranial portion of the duodenum (figure 1).
●The midgut gives rise to the caudal portion of the duodenum, the jejunum, ileum, the
ascending colon, and two-thirds of the transverse colon (figure 2A-B).
●The hindgut is the precursor of the distal one-third of the transverse colon, the
descending colon, the rectum, and the urogenital sinus (figure 3).
Anatomic and functional maturation of the gastrointestinal tract
As the process of maturation proceeds, the mucosal surface of the intestine rapidly
increases and folds to form villi. As a general rule, maturation tends to occur along
craniocaudal and proximodistal axes (table 1). Each step of development can be
influenced by a variety of processes, including genetic endowment; the biologic clock;
cellular, neural, and hormonal regulatory mechanisms; and the environment [1], which
includes the microbiota [2]. On a cellular level, these mechanisms most likely are
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regulated by the homeobox (Hox) genes, cell-to-cell interactions, epithelial-

mesenchymal interactions, and transcription factors.
Determination of the specific program of an intestinal region (ie, anterior, mid, or
posterior) occurs first, followed by detailed differentiation within that region [3]. The
signal pathways for midgut development may be a default pathway [4], with plasticity
imposed on the anterior or posterior regions by Hox genes. It is in these areas that
more specialized organs develop (eg, stomach and distal colon, respectively).
The duodenum is another specialized area of the intestine. Not only does it have a
characteristic shape, but also, its epithelium has fewer goblet cells and more
enterocytes with greater absorption than other parts of the intestine. It is the site of
many enteroendocrine cells, which secrete a variety of gut hormones. Furthermore,
buds develop from the mid-duodenum that develop into the pancreatic duct and biliary
tree (figure 4).
The duodenum is a common site for congenital malformations. Duodenal atresia and
duodenal stenosis are frequent causes of congenital intestinal obstruction, especially in
infants with Down syndrome. (See "Intestinal atresia".)
Studies in human organoids derived from induced pluripotent stem cells obtained from
patients with rare genetic defects have elucidated the transcription factors that
determine this specialization. Intestinal organoids from patients with mutations in both
alleles of PDX1 showed a loss of duodenal enteroendocrine cells compared with
controls [5]. Another patient presenting with duodenal atresia was identified as having
mutations in both alleles of RFX6 [6]. The derived organoids showed lack of
suppression of goblet cell numbers, loss of enteroendocrine cell numbers, and impaired
lipid absorption compared with control organoids. The initiation and continuation of
duodenal patterning were deranged. Correcting the mutation in situ using clustered
regularly interspaced short palindromic repeats (CRISPR) technology reversed the
deficiencies in the RFX6 mutation endoderm.
The genes regulated by RFX6 included PDX1, explaining some of the actions of RFX6.
However, other changes in the intestine were independent of PDX1. These included
those involved in signal transduction pathways important in gut tube patterning such
as the WNT and Hedgehog gene families.
Thus, RFX6 is a master regulator of duodenal specialization and the characteristics of
Mitchell-Riley syndrome (a recessive condition with mutations in RFX6) are now known.
However, the molecular pathways underlying duodenal atresia in Down syndrome
remain unexplained because neither PDX1 nor RFX6 are housed on chromosome 21.

LEFT-RIGHT ASYMMETRY
Development of the digestive organs
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The asymmetry of the contents of the abdomen is more obvious than in any other part
of the body. Only in congenital disorders of the heart are the clinical consequences of
deranged asymmetry greater than in the GI tract (figure 5).
Examples of disorders that may be caused by disturbances of lateral development
include:
●Situs inversus abdominus

●Polysplenia or asplenia

●Pancreas divisum or annular pancreas (figure 4) (see "Pancreas divisum: Clinical

manifestations and diagnosis")
●Malrotation (see "Intestinal malrotation in children")

A series of genes (Lefty, Nodal, and Pitx2) regulate lateral development. They, in turn,
are controlled by Gaf1, a member of the transforming growth factor beta (TGFB) gene
family. Pitx2 (and its partner, Isl1) has been identified in the dorsal mesentery, which
anchors the gut to the embryo. It is in this area that extracellular matrix proteins first
show asymmetry, tilting the gut to the left [7], the side in which Pitx2 expression is
greater. The Pitx2 control of the development of the cecum also involves fibroblast
growth factors [8]. It has become increasingly apparent that Pitx2 is not sufficient in
itself to control left-right asymmetry. Hyaluronan, an extracellular matrix
glycosaminoglycan, plays a critical role [9]. Hyaluronan molecules on the right side of
the embryo become covalently modified with peptides, requiring the enzyme TGFB-
related secreted protein 6, encoded by Tsg6. Lack of expression of Tsg6 results in a
failure to modify the hyaluronan and a consequent lack of coordinated asymmetry.
Furthermore, nascent hyaluronan on the left is required for full Pitx2 expression on that
side.
Pitx2 has a second action, detected in both mouse and chick [10]. The right-sided
expansion is mechanically sensed to induce TGFB. The TGFB-dependent Pitx2
expression then acts to condense mesenchyme in the left dorsal mesentery, resulting in
increased tissue stiffness on this side. Thus, the initiation of rotation depends on two
active mechanisms at the dorsal mesentery: expansion on the right and tissue
condensation on the left.
Other intracellular events are not fully elucidated but involve hedgehog (Hh) proteins
and retinoic acid [11]. Primary ciliary dyskinesia also is associated with situs inversus
but through different mechanisms. (See "Primary ciliary dyskinesia (immotile-cilia
syndrome)".)
Mechanistic studies, such as those described above, are only possible in laboratory
animals. However, messenger ribonucleic acid (mRNA) sequencing has been performed
at a cellular level in both time and space in human fetal tissue [12,13]. The resulting
atlases describe the expression of genes in every tissue of the GI tract throughout
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development. This method assumes that the detection of the transcripts correlates with
the expression of the active proteins. These data present the opportunity for future
research that triangulates mechanistic studies in mice or chicks with these human RNA-
sequencing atlases. If the developmental regulation of a gene of interest observed in
mechanistic animal studies correlates with that of the human mRNA from that gene in
the sequencing studies [12,13], this supports the relevance of the animal studies to
human development. Such an association also negates that concern that the atlas
describes only the RNA transcribed by that gene and not the protein.
Nevertheless, the function of genes that control left-right asymmetry are not the only
factors required for successful elongation and rotation of the developing intestine.
Blocking the electron transport chain (ETC), which generates adenosine triphosphate
(ATP) in aerobic cells, caused gut malrotation in amphibians, as shown by experiments
in which two separate ETC inhibitors had this effect in Xenopus [14]. One might, at first,
think that this is due to a lack of ATP supplying the energy needed to achieve the
mechanical rearrangements. However, pretreating the animals with antioxidants
removed the deleterious effects of the ETC inhibitors. The ETC's control of redox
potential in cells involved in rotating the gut may, therefore, be important. Either way,
successful rotation and elongation of the gut depend on metabolic pathways (which
may be subject to environmental insults) in addition to the proper expression and
activity of genes.

VASCULARIZATION
The supportive elements that will provide the vascular supply, the neural and hormonal
regulation, and the host defenses of the GI tract evolve concurrently with its anatomic
development. The arterial bed develops as three ventral outbuddings from the aorta to
form the celiac axis and the superior and inferior mesenteric arteries (figure 6).
Mesenteric blood flow is regulated at two points (the arteriole and the precapillary
sphincter) and controlled at two levels (intrinsic and extrinsic). Intrinsic control by local
factors regulates blood flow in response to changes in arterial pressure and tissue
oxygenation, such as those caused by vascular constriction or feeding. Extrinsic
regulation is mediated by sympathetic input from the splanchnic nerves.
Several other factors are important. Circulating endogenous and exogenous factors (eg,
hormones) may modulate vascular tone. The mesenteric blood flow also exhibits
"autoregulatory escape," which refers to the restoration of gut blood flow in the face of
extrinsic regulation [15]. When gut blood flow is decreased artificially by stimulating
periarterial mesenteric nerves (ie, the extrinsic system of control) or by infusing
norepinephrine, blood flow is restored within minutes by the intrinsic system of control,
which is triggered by local changes (eg, tissue hypoxia). The clinical advantages of this
phenomenon have long been debated, but it is likely that they relate to the unique
functions of the mesenteric vasculature. The mesenteric venous system not only
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removes the products of tissue metabolism (as do other vascular beds), but it also
transports molecules and electrolytes that have been absorbed by the intestine. An
escape from arteriolar constriction will enhance the distribution of absorbed nutrients
at a time when blood flow would otherwise have been reduced by increased systemic
sympathetic activity.

DIGESTION AND ABSORPTION

Both digestive and absorptive functions of the intestine are present at term in the
human neonate. This is also true of the villous architecture, which greatly increases the
intestinal surface area. Abnormal villous formation will result in intestinal failure,
necessitating parenteral nutrition. (See "Pathophysiology of short bowel syndrome".)
●Brush border enzymes – Disaccharidases expressed in the brush border become
active in mid-gestation and are all active during infancy in healthy children. Because
lactase activity in the fetus increases late in gestation, premature infants born at 28 to
32 weeks of gestation have reduced lactase activity. After approximately five years,
lactase activity declines in many racial groups as part of a normal process of gene
inactivation. (See "Lactose intolerance and malabsorption: Clinical manifestations,
diagnosis, and management", section on 'Developmental lactase deficiency' and
"Lactose intolerance and malabsorption: Clinical manifestations, diagnosis, and
management", section on 'Primary lactose malabsorption'.)
●Absorption – Active electrogenic transport of glucose is present in the human fetal
small intestine due to the high-affinity sodium-dependent system (the SGLT1 co-
transporter) [16]. The duodenum-to-ileum gradient of glucose absorption is established
between the 17th and 30th weeks of gestation. The developmental expression of
facilitated glucose transporter isoform GLUT2, which is responsible for exit of glucose
across the basolateral membrane, follows that of SGLT1. Amino acid transporters follow
a similar developmental trajectory and are fully active at birth.
Prenatal expression of genes that code for nutrient transporters and disaccharidases
occurs in both the colon and small intestine, but the expression disappears from the
colon during the third trimester when the villous structure of the colon turns into a flat
mucosa.
●Villous morphogenesis – Hedgehog (Hh) proteins are involved in the molecular
regulation of villous morphogenesis. Together with bone morphogenetic protein and
platelet-derived growth factor, their signaling pathways direct mesenchymal cells into
organized clusters. These cell clusters, in turn, form the site from which villi develop
[17]. Conditionally deleting negative regulators of Hh signaling in the intestinal
mesenchyme of mice [18] showed that Hh proteins acted on a set of transcription
factors, termed glioma-associated oncogene (GLi). GLi acts on two adhesion molecules
(Dachsous and Fat) that control mesenchymal clustering. Although it is not clear how

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these events interact with proteins whose defects cause congenital enteropathies, like
microvillous inclusion disease and tufting enteropathy, the molecular basis of the
initiation of villous formation has now been elucidated. (See "Approach to chronic
diarrhea in neonates and young infants (<6 months)", section on 'Congenital diarrheas
and enteropathies'.)
●Tracheal-esophageal separation – Hh and GLi are central to another important
developmental process: the separation of the trachea and esophagus, which occurs
between 25 to 35 days gestation in the human fetus. Disruption of this process results
in tracheoesophageal anomalies, including tracheoesophageal fistula (see "Congenital
anomalies of the intrathoracic airways and tracheoesophageal fistula"). In Xenopus and
mouse models, the Hh/GLi signals regulate multiple steps of tracheoesophageal
separation [19], especially the activation of a GTPase (Rab11), which is crucial in
generating a tracheoesophageal cleft, an essential step in the separation of the two
structures.
Because the respiratory system is much younger in evolution than the GI tract, proteins
such as Hh, GLi, and others must have been repurposed to regulate the development of
the respiratory system when animals evolved to live on land. It is tempting to speculate
that tracheoesophageal defects in human infants result from the relatively recent
adoption of these proteins to regulate the ontogeny of an evolutionarily novel organ,
which is not always successful. The high prevalence of tracheoesophageal defects
(whose normal development depends on repurposed regulators of development)
compared with the low prevalence of defective villous formation (whose normal
developmental pathways existed early in the evolution of the animal kingdom) adds
weight to this possibility.

NEURAL AND MOTOR FUNCTION

The neural structures of the alimentary tract are formed when neural crest cells migrate
into the rapidly growing gut. Precursors migrate from the embryonic central nervous
system [20]. The neural crest cells and muscle cells differentiate to form the three layers
of muscle that surround the mucosa and the neural network that regulates its function.
Control of motor function is provided primarily by the enteric nervous system (a
subsystem of the autonomic nervous system), which is composed of a variety of
plexuses of nerve cell bodies and interneuronal circuits. Immunohistochemical staining
demonstrates the presence of neurotransmitters by 24 weeks gestation, but the adult
distribution may not be achieved until near term. Abnormalities in the migration and
differentiation of neural crest cells result in an array of GI problems, including [21,22]:
●Hirschsprung disease (see "Congenital aganglionic megacolon (Hirschsprung
disease)")

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●Waardenburg-Shah syndrome (pigmentary abnormalities in association with

aganglionic megacolon; this condition is also called Waardenburg syndrome type IV and
Waardenburg-Hirschsprung disease) (see "The genodermatoses: An overview", section
on 'Waardenburg syndrome')
●Haddad syndrome (with congenital central hypoventilation syndrome; this condition is
also called Ondine-Hirschsprung syndrome) (see "Congenital central hypoventilation
syndrome and other causes of sleep-related hypoventilation in children")
●Intestinal neuronal dysplasias (see "Functional constipation in infants, children, and
adolescents: Clinical features and diagnosis", section on 'Other causes')
●Chronic intestinal pseudo-obstruction (certain congenital forms) (see "Chronic
intestinal pseudo-obstruction: Etiology, clinical manifestations, and diagnosis", section
on 'Genetic')
Motor activity is immature in the preterm infant. The sucking mechanism does not
appear until 32 to 34 weeks gestation [23]. Regulation of lower esophageal sphincter
tone and small intestinal motor contractions are also immature and continue to develop
into adulthood [24,25]. Gastric contents are emptied more slowly in preterm infants
than in term infants, and small intestinal transit is slower [26].

HORMONAL REGULATION
Glucocorticoids and thyroid hormone interact with cellular signals in the maturation of
the intestinal epithelium [27]. Numerous regulatory gut peptides are also produced in
the developing GI tract. Some of these peptides function as true hormones (eg, gastrin,
cholecystokinin, motilin, pancreatic polypeptide, and somatostatin), whereas others
have paracrine or neurocrine function (eg, gastric inhibitory peptide, bombesin,
vasoactive intestinal polypeptide, neurotensin, enteroglucagon, and peptide YY). All of
these peptides are present by the end of the first trimester in the fetus, but adult
distribution may not be established until term [28].
Many of these hormones are released in response to feeding. The release of some of
these is limited in the newborn compared with the adult [28,29]. In older (prepubertal)
children, GI hormones have been implicated in the development of obesity [30]. For
example, glucagon-like peptide-1 (GLP-1) has an inverse relationship to body mass
index and waist circumference. GLP-2A, which is cosecreted with GLP-1 [31], markedly
increases intestinal mass. Analysis of the molecule has resulted in the production of
teduglutide as a treatment for short bowel syndrome. (See "Management of short
bowel syndrome in children", section on 'Pharmacologic therapy'.)

HOST DEFENSE

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Many aspects of host defense are mechanical in nature and appear early in gestation.
Mucus production, for example, is present in the very preterm infant. Transcription
factors involved in early ontogeny, such as FOXQ, regulate genes that control mucin
expression [32]. On the other hand, gastric emptying and peristalsis, which prevent
stasis of intestinal contents, appear later and may not be fully functional in the preterm
infant.
T cells and B cells are produced as early as 14 weeks gestation [33]. However, antigenic
stimulation of the lamina propria cells does not occur until after birth [34]. Secretory
immunoglobulin A (IgA) is present in very low concentrations in fetal life as the fetal
intestine has few IgA-producing plasma cells. Therefore, preterm infants are unable to
form antibodies to exogenous protein [35]. However, the production and release of
cytokines are brisk.
Until the advent of technologies able to identify microbiota with rapid deoxyribonucleic
acid (DNA) sequencing (which allows detection of nonculturable bacteria), the gut was
believed to be sterile in utero. Bacteria have been identified in both placenta and
amniotic fluid in utero [36,37], although this is not universally accepted [38]. While the
major phase of bacterial colonization begins at birth, the pattern of bacteria (at least in
the meconium of infants born by caesarian section) is influenced by maternal
intrauterine bacteria [39]. A variety of other factors influence colonization, including
mode of delivery, type of feeding, and use of antibiotics [40]. In healthy infants, aerobic
organisms become abundant within a few hours and anaerobic organisms by 24 hours
[41]. These organisms are capable of metabolizing bile acids, nonabsorbed proteins,
lipids, and carbohydrates. Thus, they potentially may play an important role in the
processing of nutrients in preterm infants. (See "Human milk feeding and fortification
of human milk for premature infants", section on 'Benefits of mother's milk'.)
In addition, the microbiota directs the maturation of the host immune system, including
direct interaction with dendritic cells [42] and the regulation of T cell maturation [43,44].
These create reciprocal interactions between the microbiota and the immune system
[45-47]. (See "An overview of the innate immune system", section on 'The microbiome'.)

SUMMARY
●Anatomic maturation

•Cephalocaudad differentiation – The first steps in gastrointestinal (GI) development

involve the formation of the foregut, midgut, and hindgut from the embryonic gut tube
(figure 1 and figure 3 and figure 5). (See 'Cephalocaudad differentiation' above.)
•Lateralization – Lateralization occurs in the developing embryo to form distinct left-
right asymmetry. Some of the genetic and cellular mediators involved in lateralization
have been identified. Disorders of lateralization include situs inversus abdominus,

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malrotation of the gut, and some congenital malformations of the pancreas and spleen.
(See 'Left-right asymmetry' above.)
•Vascularization – The arterial supply to the gut develops as three ventral outbuddings
from the aorta to form the celiac axis and the superior and inferior mesenteric arteries
(figure 6). Mesenteric blood flow is subject to extrinsic and intrinsic regulation; intrinsic
regulation may compensate for extrinsic disturbances in a process termed
"autoregulatory escape." (See 'Vascularization' above.)
●Functional maturation

•Digestion and absorption – The molecular basis determining the development of villi
has been elucidated and uses some of the same regulatory proteins that are involved in
the separation of the trachea from the intestine in early fetal life. (See 'Digestion and
absorption' above.)
•Motility – Control of motor function is provided primarily by the enteric nervous
system (a subsystem of the autonomic nervous system). Abnormalities in the migration
and differentiation of neural crest cells result in an array of GI problems, including
Hirschsprung disease. (See 'Neural and motor function' above.)
•Gut regulatory hormones – Regulatory gut peptides that are produced in the
developing GI tract include gastrin, cholecystokinin, motilin, pancreatic polypeptide,
and somatostatin, as well as some paracrine or neurocrine mediators. All of these
peptides are present by the end of the first trimester in the fetus, but adult distribution
may not be established until term (table 1). (See 'Hormonal regulation' above.)
•Gut immune defense – The development of immune defenses in the gut is distributed
across embryonal maturation and continues to develop after birth. Preterm infants
have immature gut defenses because of decreased motility and reduced secretion of
IgA. (See 'Host defense' above.)
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Contributor Disclosures
Ian R Sanderson, MDNo relevant financial relationship(s) with ineligible companies to
disclose.Melvin B Heyman, MD, MPHEquity Ownership/Stock Options: Amgen [Inflammatory
bowel disease]. Grant/Research/Clinical Trial Support: AbbVie [Inflammatory bowel disease];
Arena [Inflammatory bowel disease]; Janssen [Inflammatory bowel disease]; Lilly
[Inflammatory bowel disease]; Pfizer [Ulcerative colitis]; Takeda [Inflammatory bowel disease].
Consultant/Advisory Boards: AbbVie [Constipation]. All of the relevant financial relationships
listed have been mitigated.Alison G Hoppin, MDNo relevant financial relationship(s) with
ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When
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Conflict of interest policy

Graphics

Anatomic and functional maturation of the gastrointestinal tract

Postconceptional age
20 weeks 25 weeks 30 weeks 35 weeks 40
weeks
Mouth Salivary glands Swallow reflex Lingual lipase Sucking reflex
present present

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

Esophagus Muscle layers present Striated Poor lower

epithelium esophageal
present sphincter tone
Stomach Gastric glands G cells appear Gastric secretions Slow gastric *
present present emptying
Pancreas Exocrine and Zymogen Reduced trypsin, *
endocrine tissue present lipase
differentiate
Liver Lobules form Bile secreted Fatty acids absorbed *
Intestine Crypts and villi form Glucose Dipeptidese, Lactase active
transport sucrase, and maltase
present active
Colon Crypts and villi Meconium
recede passed
Italics indicate functional maturation.
* Full functional maturation occurs postnatally.
Reproduced with permission from: Berseth, CL. Developmental Anotomy and Physiology of the Gastrointestinal Tract. In:
Avery's Diseases of the Newborn, 7th ed, Taeusch HW, Ballard RA (Eds), W.B. Saunders Company, Philadelphia, 1998. Table
78-12. Copyright 1998 W.B. Saunders.
Graphic 65282 Version 1.0

Foregut formation

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

Formation of a ventral mesentery in the foregut region. The accessory organs of digestion
(liver, pancreas, and gallbladder) derive from the foregut only. Like the gut tube, they rest in a
"sling" of mesoderm, but because the gut tube already occupies the dorsal mesentery, these
organs need a mesentery of their own. The ventral mesentery appears to form from thinning
of the overlying mesoderm of the septum transversum.
Reproduced with permission from: Sadler TW. Langman's Medical Embryology, 9th Edition Image Bank. Baltimore:
Lippincott Williams & Wilkins, 2004. Copyright © 2004 Lippincott Williams & Wilkins.
Graphic 60244 Version 1.0

Normal rotation of the duodenojejunal loop

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

(A) The midgut forms a slight bend ventrally.

(B) The duodenojejunal junction rotates 90 degrees counterclockwise (to the right of the
superior mesentery artery [SMA]).
(C) The duodenojejunal junction continues to rotate counterclockwise around the SMA (now
180 degrees from its original position).
(D) In its final position, the duodenojejunal junction has rotated 270 degrees and lies to the
left of the SMA.
Graphic 78643 Version 2.0

Normal rotation of the cecocolic loop

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

(A) The starting point of the cecum is directly inferior to the superior mesenteric artery (SMA).
(B) The cecum has rotated 90 degrees counterclockwise.
(C) The cecum continues to rotate around the SMA, now 180 degrees from its starting point
and directly ventral to the SMA.
(D) The final position the cecum, after 270 degrees counterclockwise rotation, is to the right of
the SMA.
Graphic 68817 Version 2.0

Hindgut formation

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

A wedge of mesoderm divides the hindgut. Recall that the allantois diverticulum is trapped in
the connecting stalk (A). A migrating urorectal septum of mesoderm pinches the base of the
diverticulum off of the hindgut (B and C). This results in two portals to the outside world, one
of which is still connected to the gut tube (anal) and one of which is a blind pouch (urogenital).
Reproduced with permission from: Sadler TW. Langman's Medical Embryology, 10th Edition. Baltimore: Lippincott Williams
& Wilkins, 2006. Copyright © 2006 Lippincott Williams & Wilkins.
Graphic 81367 Version 1.0

Anatomy and embryology of pancreas divisum

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The pancreas develops from two parts whose ducts are in continuity with the common bile
duct. One part is ventral and the other dorsal to the intestinal tract before rotation. The
rotation brings the two parts together with separate ducts. The duct of the dorsal (larger) part
later becomes continuous, enters that of the ventral part which enters the duodenum with the
common bile duct. However, in a congenital malformation (pancreas divisum) the other two
parts of the pancreas remain distinct, each with its own duct.
Graphic 78995 Version 3.0

Development of the digestive organs

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Origin of the accessory organs of digestion.

(A-B) The accessory organs of digestion (liver, gallbladder, and pancreas) first emerge as buds
of the foregut tube in the space provided by the ventral mesentery.
(C-E) As the organs enlarge and move, the foregut mesentery goes with them and persists in
the same way that the dorsal mesentery does.
Reproduced with permission from: Sadler TW. Langman's Medical Embryology, 10th Edition. Baltimore: Lippincott Williams
& Wilkins, 2006. Copyright © 2006 Lippincott Williams & Wilkins.
Graphic 66413 Version 3.0

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5/29/25, 11:15 AM Overview of the development of the gastrointestinal tract

Development of the gastrointestinal vasculature

Embryo during the sixth week of development, showing blood supply to the segments of the
gut and formation and rotation of the primary intestinal loop. The superior mesenteric artery
forms the axis of this rotation and supplies the midgut. The celiac and inferior mesenteric
arteries supply the foregut and hindgut, respectively.
Reproduced with permission from: Sadler T, PhD. Langman's Medical Embryology, Ninth Edition Image Bank. Baltimore:
Lippincott Williams & Wilkins, 2003. Copyright © 2003 Lippincott Williams & Wilkins.
Graphic 80755 Version 2.0

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