Ventral Pancreatic Buds Research Articles

Development of human pancreas

Pancreas is an exocrine and endocrine organ. Exocrine portion secretes digestive fluid. Endocrine portion secreting insulin and glucagon etc. Pancreas developed from dorsal and ventral pancreatic buds, which arise from either side of distal foregut. When duodenum rotates to right, ventral pancreatic bud(VPB) rotates posterior along with common bile duct(CBD) and finally lies below and behind the dorsal pancreatic bud(DPB). In humans, DPB forms major part and VPB forms inferior part of head and uncinate process of pancreas. Main duct (Duct of Wirsung) is derived from whole of ventral pancreatic duct(VPD) and distal part of dorsal pancreatic duct(DPD). Main duct joins with CBD and it perforated posteromedial side of second part of duodenum at major duodenal papilla. Occasionally accessory duct might originate from proximal part of DPD and open into minor papilla. Sometimes two buds do not fuse and lead to pancreatic divisum. Abnormal rotation and fusion of buds might lead to annular pancreas. A few endodermal pancreatic evaginations may remain and migrate in bowel wall and form accessory(heterotopic) pancreas. Islets originating from DPB have more insulin synthesis. Neck, body and tail of pancreas is supplied by coeliac trunk. Derivatives of right VPB are supplied by branches of superior mesenteric artery. During rotation of VPB, superior mesenteric vessels(SMV) were engaged in between DPB and VPB. Lastly, SMV is located posterior to neck but it is anterior to uncinate process of pancreas. Detailed study of development of exocrine and endocrine portions is required for successful management of pathology of the pancreas.

Surgical management of portal annular pancreas

Background: Portal annular pancreas is a rare congenital abnormality in the fusion of the dorsal and ventral pancreatic buds during gestation. In these cases, the uncinate process lies posterior to the portal vein and fuses with the body of the pancreas. This creates a circumferential encasement of the portal vein and three variations of the pancreatic duct anatomy have been described to be associated with this anatomic variation. In this video, we discuss the surgical management a healthy female with no past medical, surgical, alcohol, or endoscopic history who presented with recurrent pancreatitis and a diagnosis of a high-risk IPMN.

S1888 A Curious Case of Recurrent Pancreatitis: A Case Report

Introduction: Annular pancreas, a congenital anomaly characterized by incomplete rotation of the ventral pancreatic bud, causes a ring of pancreatic tissue to encircle the duodenum. It is commonly accompanied by pancreatic divisum, which occurs when the main pancreatic duct and accessory duct fail to fuse. Patients often present with recurrent pancreatitis due to partial obstruction of the pancreatic duct caused by fibrosis. Case Description/Methods: A 72-year-old Caucasian male presented with recurrent episodes of acute pancreatitis. A CT abdomen (Figure A) revealed pancreatic tissue surrounding the second portion of the duodenum consistent with an annular pancreas. A pancreatic duct stone was also noted. An MRCP (Magnetic resonance cholangiopancreatography) was consistent with annular pancreas with persistent dilation of the main and accessory pancreatic ducts and a 6mm stone noted in the pancreatic duct (Figure B). On an initial ERCP (Endoscopic retrograde cholangiopancreatography), the pancreatic duct could not be cannulated through the major papilla and minor papilla could not be identified due to inflammation. An EUS (Endoscopic ultrasound) was performed, which was suggestive of pancreas divisum. The minor papilla was cannulated, and a stent was placed in the pancreatic duct. In a subsequent ERCP (Figure C), the patient had the pancreatic stone removed, with complete resolution of his symptoms. Discussion: Typically, patients with annular pancreas present with symptoms during childhood. While infrequent, some patients remain asymptomatic until 20-50 years of age. This case demonstrates the potential to remain asymptomatic until even 72 years of age. Thus, it is important for physicians to be aware of the clinical manifestations of annular pancreas, as they could arise at any stage in life. By increasing awareness surrounding annular pancreas and management of its complications, we hope to increase the rate of early intervention.Figure 1.: Image 1A. Contrast-enhanced axial CT of the abdomen at the level of the pancreatic head. The pancreas (white bracket) is seen surrounding the 2nd part of the duodenum (white asterisk), compatible with annular pancreas. A 6 mm calcification (circled) is present in the region of the minor papilla (arrows indicating pancreatic ducts). Image 1B. Coronal MRCP images. Annular pancreas, with only a thin rim of pancreatic tissue surrounding the duodenum. The dorsal duct is best shown to wrap completely around the duodenum on MRCP images (arrow). Image 1C. ERCP fluoro image showing the previously placed pancreatic duct stent (which does appear to have a loop-like configuration) and the pancreatic stone.

A RARE CASE OF A 27-YEAR-OLD FEMALE PRESENTED WITH DUODENAL OBSTRUCTION DUE TO ANNULAR PANCREAS

Background. Annular pancreas is a rare congenital abnormality characterized by a ring of pancreatic tissue surrounding the descending portion of the duodenum. It is thought to originate from the incomplete rotation of the ventral pancreatic bud. Objective. To present a case description of a 27-year-old female with duodenal obstruction due to annular pancreas Material and methods. The clinical manifestations, laboratory and instrumental findings of a female patient. Results. We report the case of a 27-year-old female with 3 months history of upper abdominal pain, nausea, postprandial fullness, and recurrent vomiting. Physical examination revealed nothing except for the thin-built body. Routine biochemical and hematological investigations were within normal limits. The patient's standing direct abdominal graphy revealed air-fluid level and dilated both stomach and the first part of duodenum. Upper gastrointestinal series showed circumferential extrinsic compression on the 2nd portion of the duodenum. Abdominal computerized tomography (CT) and ultrasonography (USG) revealed a ring of pancreatic tissue encircling the second part of the duodenum. We present the clinical presentation, treatment plan which is performed through a duodenojejunostomy bypass procedure, and follow-up of the patient. Conclusions. Annular pancreas is associated with duodenal atresia. It usually appears in infancy but might become clinically evident in adulthood with obstruction of the duodenum. The symptoms include constipation, nausea, and vomiting. and usually arise due to obstruction to gastric emptying. In order to confirm the presence of annular pancreas, abdominal CT scans with high resolution and angiography protocols as well as magnetic resonance imaging are helpful.

Bisection, Disjuncture, Aqueduct: Pancreas Divisum

The conformable congenital anatomic malformation of the pancreas is Pancreas Divisum. Conventionally, the pancreas evolves from the fusion of the dorsal and the ventral pancreatic buds throughout the sixth week of gestation. The dorsal bud structures the head, tail and the body of the pancreas while the ventral bud configures the uncinate process besides the inferior portion of the head. The concurrence of this arrangement permits the amalgamation of the ductal schemata so the major pancreatic duct evacuates the pancreatic secretions into the duodenum through the major duodenal papilla. Comparatively 30% of entities delineate the traditional anatomical derivatives, where the proximal dorsal pancreatic duct prevails as the accessory pancreatic duct and expels through the minor duodenal papilla.

A rare congenital anomaly of the duodenal shape incidentally found at duodenopancreatectomy: A case report and literature review.

IntroductionAn anomaly of the duodenal shape is one of the rare congenital anomalies and remains poorly known in many previous studies and the literature. The duodenum is formed by developing the terminal foregut and proximal midgut through four stages in the embryonic period. According to the anatomy, the duodenum is typically described as C–shaped, U–shaped, or even horseshoe-shaped.Presentation of caseThe patient was hospitalized for abdominal pain and jaundice and diagnosed with ampullary carcinoma. During surgery, we incidentally discovered that the duodenum was not a C-shape. The first part of the duodenum and proximal half of the second part descended the head of the pancreas. However, the distal half of the second part bent to the right and ascended upwards to the upper-right margin of the pancreatic head. After that, the third part ran slantingly downward to the left and posterior of the pancreas and portal vein.DiscussionDuring the fifth week, the ventral pancreatic bud moves around the duodenum's posterior side and unites the dorsal pancreatic bud at the sixth week. The place of the distal half of D2 migrated abnormally after ventral pancreatic bud rotation finished. The rapid and premature elongation of the proximal midgut, the influence of a very fast enlarged liver, or the early return of the umbilical loop combine with insufficiently developed abdominal space. These reasons may have led to the abnormal folding of the D2 position.ConclusionKnowledge about this anomaly helps clinicians know the duodenal-anatomical abnormalities.

Annular Pancreas with Meckel’s Diverticulum and Ladd’s Band in Neonate

Annular pancreas is a rare congenital malformation consisting of pancreatic tissue surrounding the descending portion of the duodenum and induces intestinal obstruction. This is caused by incomplete rotation of the ventral pancreatic bud. In children, the annular pancreas is also associated with trisomy 21 and other congenital diseases such as Meckel’s diverticulum, intestinal, or cardiac malformations. Here we presented a rare case of the annular pancreas with Meckel’s diverticulum identified by the abdominal exploration of an 8-day-old girl who suffered from projectile bilious vomiting. A plain abdominal radiograph showed a ‘double-bubble sign’ with air in the stomach and duodenum, and the upper gastrointestinal series showed a dilated proximal duodenum, with partial obstruction of the descending duodenum. The exploration revealed an annular pancreas, Meckel’s diverticulum, and Ladd’s band without large bowel malrotation. Subsequently, she ate well and was discharged on the 27th hospital day.

Portal annular pancreas: An unsual pancreatic pseudotumor with clinical significance

Portal annular pancreas (PAP) is a rare congenital anomaly due to abnormal fusion of ventral pancreatic bud left to the developing portal vein. Its incidence is 1.1%–3.4% in the literature. PAP is commonly involving the uncinate process; complete encircling is relatively rare. Proposed hypothesis for the congenital PAP is (1) hypertrophied ventral pancreatic bud fuses with the body of the pancreas left to the portal vein and (2) malformation of the portal vein. We found a bulky pancreas in a 51-year-old male during an autopsy. After careful dissection, we observed that the pancreas was completely encircling around the portal vein cranial to its formation. The encircled tissue was confirmed as normal pancreatic tissue by H and E and immunohistochemical staining. Pancreatic ductal pattern was observed anterior to the portal vein. This condition is usually asymptomatic; most of the time, the same was diagnosed incidentally during surgery. However, in cases of the malignant lesion in the head of the pancreas, the PAP is usually confused as the tumor's extension (pseudotumor). The management of posttransection pancreatic stump is challenging and usually results in complications such as pancreatic fistula. Knowledge about the PAP is necessary for the surgeon and radiologist for accurate diagnosis and prior planning to prevent the postoperative complications.

S3575 A Unique Case of Acute Pancreatitis Due to Metastaic Melanoma to the Minor Papilla in a Patient With Pancreas Divisum

INTRODUCTION: Metastatic melanoma can occur in the gastrointestinal tract in patients with diagnosed metastatic malignant melanoma. We present a case of metastatic melanoma to the duodenum and minor papilla in a patient with pancreas divisum, which served as a trigger for acute pancreatitis. CASE DESCRIPTION/METHODS: A 54 yr old male presented to the emergency department with severe abdominal pain, elevated lipase 1654 U/L (0–60) and mildly elevated liver function tests (AST 40 IU/L (14–30) ALT 55 IU/L (10–52)). CT scan showed a metastatic process involving the pancreas, liver, lungs, and also worsening pancreatic duct dilation (7 mm) compared to the previous CT scan three months prior. His past medical history was significant for melanoma of the right thumb s/p amputation, metastatic melanoma (BRAF V600E negative), tobacco abuse, and recent 20 pounds weight loss. Gastroenterology was consulted for acute pancreatitis and recommended an EUS and ERCP. EUS detected multiple hypoechoic round and oval masses within the pancreatic and liver parenchyma suggesting metastasis, and also pancreas divisum, with pancreatic duct measuring 5 mm in diameter. On ERCP, the major papilla and the main biliary duct were normal. However, on the endoscopic view, we detected many 3–10 mm black and flat infiltrative masses in the first and second portion of the duodenum, very suggestive of duodenal metastasis. One of the flat masses was found in the minor papilla. Subsequently the dorsal pancreatic duct was unable to be cannulated. Supportive care was recommended and he was discharged in stable medical condition. DISCUSSION: Metastatic melanoma metastasizes to the GI tract between 1-4% of patients with diagnosed metastatic malignant melanoma. Our patient had multiple metastasis visualized in the duodenum, a common site of tumor occurrence. The patient also had pancreatic divisum, previously undiagnosed and seen on EUS. These patients have a failure of the dorsal and ventral pancreatic buds fusing and thus result in majority of the pancreas draining through the dorsal duct of Santorini through the minor papilla. The abnormal fusion causes abnormal drainage of the majority of the pancreatic juice into the naturally narrowed minor papilla, causing elevation of intraductal pressure in some patients. Our patient had no prior episodes of pancreatitis prior to his metastatic melanoma diagnosis, making the melanotic lesion the likely culprit in this case for the occurrence of acute pancreatitis.Figure 1.: Minor Papilla with Metastatic Melanoma Lesion.Figure 2.: Multiple Metastatic Melanoma Lesions in Duodenum.Figure 3.: Normal Major Papilla.

Incidental Finding of Annular Pancreas in a Routine Cadaveric Dissection: Case Report

AbstractAnnular pancreas is a rare congenital anomaly that results from the malrotation of the ventral pancreatic bud. The presentation of annular pancreas varies: it can be asymptomatic or present clinical symptoms of duodenal obstruction that can affect all age groups, from newborns to adults. In the present case report, we describe a complete type of annular pancreas at the level of the second part of the duodenum, which was an incidental finding in a prosected specimen. This anomaly has significant clinical relevance to clinicians and radiologists due to its variable presentation. The embryological, clinical and radiological aspects of this congenital anomaly are discussed in detail in the present article.

Mypt1 regulates Bmp signaling to promote embryonic exocrine pancreas growth in zebrafish.

Myosin phosphatase targeting subunit 1 (Mypt1) is the regulatory subunit of myosin phosphatase which dephosphorylates the light chain of myosin II to inhibit its contraction. Although biochemical properties of Mypt1 have been characterized in detail, its biological functions in organisms are not well understood. The zebrafish mypt1 sq181 allele was found defective in the ventral pancreatic bud and extrapancreatic duct development, resulting in dysplasia of exocrine pancreas. In mypt1 sq181 mutant, the early growth of the ventral pancreatic bud was initiated but failed to expand due to impaired cell proliferation and increased cell apoptosis. As Mypt1 is essential for cell migration, the loss-of-function of Mypt1 in the mutant disrupted the lateral plate mesoderm migration during gut looping, therefore, altering the Bmp2a expression pattern within it, and eventually leading to impaired Bmp signaling in the adjacent exocrine pancreas. Overexpression of bmp2a could rescue the development of exocrine pancreas, suggesting that the impaired Bmp2a signaling is responsible for the pancreatic development defects. Bmp2a has been reported to promote the early specification of the ventral pancreatic bud, and our study reveals that it continues to serve as a cell proliferation/survival signal to ensure pancreatic bud growth properly in zebrafish.

Histomorphometry of pancreas development in hybrid chicken (Galus galus) embryo and fetus.

The pancreas comprises an important metabolic organ of endocrine and exocrine character that has embryonic origin of rudimentary buds that fuse to form the organ. The present work aims to describe the pancreatic histogenesis of hybrid chick embryos (Gallus gallus). The research was performed in the UFPI, previously approved by the CEUA with protocol no. 040/15. We used 120 fertilized eggs of hybrid chickens kept in an incubator with controlled temperature and humidity. Daily collections of embryos and fetuses were performed from 4 to 21 days of incubation through the anatomical dissection consecutive the euthanasia. The tissues, previously fixed in 10% buffered formaldehyde, were submitted to histological processing and stained with hematoxylin-eosin. Finally, the mounted slides were analyzed in image software to obtain histomorphometric data, which were submitted to statistical analysis. The pancreas of hybrid chicken embryos originates around the fourth day of incubation with the dorsal and ventral pancreatic bud formation, which are composed by epithelial and mesenchymal cells. These cells differ in exocrine and endocrine cells. Around twelve embryonic days occurs the buds fusion and the immature organ formation that will give continue with the ductal system development, vascularization and compartmentalization of the endocrine and exocrine parts. Until 21st day of incubation it is possible to identify undifferentiated tissue forms which suggesting postnatal histogenesis. The description of pancreas histogenesis using histometric data on hybrid chicken embryos contributes to the clarification of embryonic development and reaffirms the premise that chickens serve as an experimental model for embryonic study of mammals.

Annular pancreas presenting as gastric outlet obstruction in an adult: a case report

Annular pancreas is a rare congenital abnormality which arises in the embryo by persistence of pancreatic tissue in the track which the ventral pancreatic bud follows in its rotation round the duodenum. A 21 years old male was admitted because of a non bilious vomiting and epigastric fullness after intake of food. Diagnosis was confirmed with contrast enhanced CT scan of the abdomen. He successfully underwent laparoscopic gastrojejunostomy with uneventful postoperative recovery. Though rare, annular pancreas should be considered as differential diagnosis in patient presenting as gastric outlet obstruction after excluding common causes.Journal of Society of Surgeons of NepalVol. 17, No. 2, 2014, Page: 35-36

A rare congenital anomaly of the pancreas: a cadaveric case report.

The pancreas is formed by ventral and dorsal pancreatic buds which arise from the endodermal lining of the gut. When the duodenum rotates to the right, the ventral pancreatic bud migrates dorsally and finally come and lie below the dorsal pancreatic bud. The developmental errors in the rotation of these components lead to annular pancreas. We report a rare type of the incomplete annular pancreas around the contents of right free margin of lesser omentum. There was an extra pancreatic mass situated horizontally immediately above the superior border of the pancreas, situated behind the lesser omentum. The right end of this mass extended into the epiploic foramen and incompletely encircled the portal vein, bile duct and hepatic artery proper from behind. The left end of the extra pancreatic mass was extended towards the lesser curvature of the stomach. Further, this mass completely surrounded the origin of three branches of the celiac trunk. Its right end was found to be continuous with the head of the pancreas, close to the pylorus. Histology of the extra pancreatic mass revealed the presence of normal pancreatic tissue. preoperative diagnosis of this rare anomaly is of clinical importance during surgeries involving the contents of right free margin of lesser omentum and epiploic foramen.

Pancreas divisum: a common developmental variant that deserves attention in preclinical medical education.

Clinical literature indicates that pancreas divisum (PD) is present in 3-22% of the population and may be associated with an increased risk of pancreatitis. PD is a developmental variant wherein the duct systems derived from the dorsal and ventral pancreatic buds are not fused. Hence secretions from the head, neck, body, and tail, which develop from the dorsal bud, must pass through the minor duodenal papilla. The smaller uncinate process, derived from the ventral bud, drains through the major duodenal papilla. The purpose of this study was: (1) to do a cadaveric dissection to confirm whether PD is common in donors who had not been selected because they had pancreatitis and (2) to determine the frequency of PD descriptions in anatomy, embryology, pathology, and surgery books in our libraries. For our anatomical study, pancreata of eight human donors were dissected. Dye was injected into the ducts so that any communications between main and accessory ducts could be easily located. For our literature review, 22 anatomy, 14 embryology, 11 pathology, and 26 surgery books were examined for mention of PD. PD was unambiguously identified in two donor cadavers. However, only 14% of the anatomy plus embryology books compared to 70% of the surgery plus pathology books describe PD. Cadaveric dissection confirms that PD is indeed prevalent. The prevalence of PD with its increased risk of pancreatitis merits inclusion of this topic in textbooks of anatomy and embryology.

Pancreatic Divisum: Beyond what is Obvious

In over 90% of healthy people, the dorsal and ventral endodermal pancreatic buds fuse to form the adult pancreas. However, in about the remaining 10% of the population where the fusion does not occur, pancreatic divisum (PD) results. This indeed is the commonest congenital anomaly of pancreas. The dorsal root usually drains a part of pancreatic head, the body and tail of the pancreas via a minor papilla into the duodenum. The ventral root drains the uncinate process and part of the pancreatic head with the CBD via the major papilla into the duodenum and the two roots are communicated with one another. In classic PD (type1) there is a complete failure of fusion of ducts, and a small ventral duct (Santorini) drains through the larger major papilla, and a larger dorsal duct (Wirsung) drains through the smaller minor papilla. In type 2, there is a complete absence of duct of Wirsung. While in type (incomplete PD), there is a filamentous or tiny caliber communication between the dominant dorsal duct of Wirsung and duct of Santorini. In the western countries, the incomplete PD is uncommon with a reported incidence of 0.13%-0.9%. However recent reports from Japan and Korea show a much higher prevalence of 48% to 52%, of incomplete PD. In patients with a large duct, the majority of the pancreatic secretions pass through the minor papilla (instead of major) resulting in inadequate drainage and pain caused by obstruction. However while these features of PD are relatively well known, there are some aspects of PD, which are not so obvious. These include its true prevalence, its role in development of pancreatitis and carcinoma of pancreas, the genetic abnormalities and its association with pancreatitis in presence of PD and the appropriate management of these patients when symptomatic

Laminin β1a controls distinct steps during the establishment of digestive organ laterality

Visceral organs, including the liver and pancreas, adopt asymmetric positions to ensure proper function. Yet the molecular and cellular mechanisms controlling organ laterality are not well understood. We identified a mutation affecting zebrafish laminin β1a (lamb1a) that disrupts left-right asymmetry of the liver and pancreas. In these mutants, the liver spans the midline and the ventral pancreatic bud remains split into bilateral structures. We show that lamb1a regulates asymmetric left-right gene expression in the lateral plate mesoderm (LPM). In particular, lamb1a functions in Kupffer's vesicle (KV), a ciliated organ analogous to the mouse node, to control the length and function of the KV cilia. Later during gut-looping stages, dynamic expression of Lamb1a is required for the bilayered organization and asymmetric migration of the LPM. Loss of Lamb1a function also results in aberrant protrusion of LPM cells into the gut. Collectively, our results provide cellular and molecular mechanisms by which extracellular matrix proteins regulate left-right organ morphogenesis.

Insulin-secreting cell regeneration: a dream or reality?

189 ISSN 1758-1907 10.2217/DMT.13.12 © 2013 Future Medicine Ltd Diabetes Manage. (2013) 3(3), 189–191 Autoimmune destruction of insulinproducing b-cells leads to Type 1 diabetes (T1D). The global challenge to find a cure for T1D centers on transplanting or regenerating insulin-producing cells, while at the same time preventing disease recurrence. This quest for cure dominates prevention in the public’s mind, although in reality there can be no cure of an autoimmune disease without prevention. The impetus comes from the demands of daily insulin injections to treat T1D and the inability of this approach to attain physiologic control of blood glucose, in many cases leading to longer-term complications secondary to hyperglycemia. Although transplantation of the pancreas or purif ied islets allows near-normal maintenance of blood glucose, it comes at a high technical and financial cost and is severely limited by the shortage of organ donors. In addition, long-term insulinindependence appears to be the exception rather than the rule [1]. Alternative sources of b-cells, primarily embryonic or adult stem/progenitor cells, have, therefore, been pursued [2–5]. Turning the dream of regenerating b-cells into a reality requires an understanding of normal b-cell ontogeny and how to mimic and evaluate it. The b-cell regeneration progress has to match the known molecular identity of a developing pancreas. Over the last 30 years, pancreatic endocrine cell lineages have been mapped through the role of specialized growth factors and sequential activation/inhibition of signaling pathways. Thus, early specification of dorsal and ventral pancreatic buds from foregut endoderm requires Hedgehog and FGF signaling [6]. Growth and branching morphogenesis involve FGF, Notch, Wnt, TGF-b and EGF pathways [7]. These pathways are activated by interactions with surrounding tissues, causing expression of specialized transcription factors. Sets of transcription factors form transcriptome signatures responsible for tissue transformation. Although incomplete, these groups are used to identify whether cultivated cells reached late-def initive endoderm, pancreatic progenitor or immature b-cell stages of development. In addition, the b-cell regeneration progress has to match known b-cell function. Cellular response to incretins, such as glucose and exenatide, is a valuable feature. It displays insulin production, reveals presence of secretory networks and detects dose-dependent insulin

Annular pancreas: A review of its molecular embryology, genetic basis and clinical considerations

The annular pancreas remains an intriguing congenital anomaly. Many theories have sought to explain its embryological basis; however, no consensus has yet been reached regarding the exact mechanism of aberration. More recently, molecular investigations have shed light on some of these theories, confirming the origination of annular tissue from the ventral pancreatic bud. These studies highlight the role of the hedgehog signaling pathway in the development of this anomaly. Overexpression of the ventral-specific gene transmembrane 4 superfamily member 3 (tm4sf3) has also been associated with annular formation. Moreover, isolated case reports of familial annular pancreas have also been documented, suggesting a genetic basis for the development of this anomaly. Annular pancreas can initially present in childhood or adulthood with symptoms of duodenal obstruction and is diagnosed using a variety of imaging modalities. Treatment usually involves surgical correction, with bypass procedures (e.g. duodenoduodenostomy, gastrojejunostomy or duodenojejunostomy) currently favored over annular resection due to complications associated with the latter approach.

Homeoprotein hhex-induced conversion of intestinal to ventral pancreatic precursors results in the formation of giant pancreata in Xenopus embryos

Liver and ventral pancreas develop from neighboring territories within the endoderm of gastrulae. ventral pancreatic precursor 1 (vpp1) is a marker gene that is differentially expressed in a cell population within the dorsal endoderm in a pattern partially overlapping with that of hematopoietically expressed homeobox (hhex) during gastrulation. In tail bud embryos, vpp1 expression specifically demarcates two ventral pancreatic buds, whereas hhex expression is mainly restricted to the liver diverticulum. Ectopic expression of a critical dose of hhex led to a greatly enlarged vpp1-positive domain and, subsequently, to the formation of giant ventral pancreata, putatively by conversion of intestinal to ventral pancreatic precursor cells. Conversely, antisense morpholino oligonucleotide-mediated knockdown of hhex resulted in a down-regulation of vpp1 expression and a specific loss of the ventral pancreas. Furthermore, titration of hhex with a dexamethasone-inducible hhex-VP16GR fusion construct suggested that endogenous hhex activity during gastrulation is essential for the formation of ventral pancreatic progenitor cells. These observations suggest that, beyond its role in liver development, hhex controls specification of a vpp1-positive endodermal cell population during gastrulation that is required for the formation of the ventral pancreas.