Talk:Endocrine - Pancreas Development
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Cite this page: Hill, M.A. (2024, April 16) Embryology Endocrine - Pancreas Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Endocrine_-_Pancreas_Development |
| About Discussion Pages |
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Glossary Links
Cite this page: Hill, M.A. (2024, April 16) Embryology Endocrine - Pancreas Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Endocrine_-_Pancreas_Development |
2010
Elevated glucose induces congenital heart defects by altering the expression of tbx5, tbx20, and has2 in developing zebrafish embryos
Liang J, Gui Y, Wang W, Gao S, Li J, Song H. Birth Defects Res A Clin Mol Teratol. 2010 Jun;88(6):480-6.
BACKGROUND: Maternal diabetes increases the risk of congenital heart defects in infants, and hyperglycemia acts as a major teratogen. Multiple steps of cardiac development, including endocardial cushion morphogenesis and development of neural crest cells, are challenged under elevated glucose conditions. However, the direct effect of hyperglycemia on embryo heart organogenesis remains to be investigated.
METHODS: Zebrafish embryos in different stages were exposed to D-glucose for 12 or 24 hr to determine the sensitive window during early heart development. In the subsequent study, 6 hr post-fertilization embryos were treated with either 25 mmol/liter D-glucose or L-glucose for 24 hr. The expression of genes was analyzed by whole-mount in situ hybridization.
RESULTS: The highest incidence of cardiac malformations was found during 6-30 hpf exposure periods. After 24 hr exposure, D-glucose-treated embryos exhibited significant developmental delay and diverse cardiac malformations, but embryos exposed to L-glucose showed no apparent phenotype. Further investigation of the origin of heart defects showed that cardiac looping was affected earliest, while the specification of cardiac progenitors and heart tube assembly were complete. Moreover, the expression patterns of tbx5, tbx20, and has2 were altered in the defective hearts.
CONCLUSIONS: Our data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5, tbx20, and has2 in the heart. We also show the first evidence that cardiac looping is affected earliest during heart organogenesis. These research results are important for devising preventive and therapeutic strategies aimed at reducing the occurrence of congenital heart defects in diabetic pregnancy.
PMID: 20306498 http://www.ncbi.nlm.nih.gov/pubmed/20306498
Fetal topographical anatomy of the pancreatic head and duodenum with special reference to courses of the pancreaticoduodenal arteries
Jin ZW, Yu HC, Cho BH, Kim HT, Kimura W, Fujimiya M, Murakami G. Yonsei Med J. 2010 May;51(3):398-406.
PURPOSE: The purpose of this study is to provide better understanding as to how the "double" vascular arcades, in contrast to other intestinal marginal vessels, develop along the right margin of the pancreatic head. MATERIALS AND METHODS: In human fetuses between 8-30 weeks, we described the topographical anatomy of the vessels, bile duct, duodenum as well as the ventral and dorsal primordia of the pancreatic head with an aid of pancreatic polypeptide immunohisto-chemistry. RESULTS: The contents of the hepatoduodenal ligament crossed the superior side of the pylorus. Moreover, the right hepatic artery originating from the superior mesenteric artery ran along the superior aspect of the pancreatic head. An arterial arcade, corresponding to the posterior pancreaticoduodenal arteries, encircled the superior part of the pancreatic head, whereas another arcade, corresponding to the anterior pancreaticoduodenal arteries, surrounded the inferior part. The dorsal promordium of the pancreas surrounded and/or mixed the ventral primordium at 13-16 weeks. Thus, both arterial arcades were likely to attach to the dorsal primordium. CONCLUSION: The fetal anatomy of the pancreaticoduodenal vascular arcades as well as that of the hepatoduodenal ligament were quite different from adults in topographical relations. Thus, in the stage later than 30 weeks, further rotation of the duodenum along a horizontal axis seemed to be required to move the pylorus posterosuperiorly and to reflect the superior surface of the pancreatic head posteriorly. However, to change the topographical anatomy of the superior and inferior arterial arcades into the final position, re-arrangement of the pancreatic parenchyma might be necessary in the head.
PMID: 20376893 http://www.ncbi.nlm.nih.gov/pubmed/20376893
http://www.eymj.org/search.php?where=aview&id=128080&code=0069YMJ&vmode=AFTR
Wolcott-Rallison syndrome
Orphanet J Rare Dis. 2010 Nov 4;5:29.
Julier C, Nicolino M.
Inserm UMR-S 958, Faculté de Médecine Denis-Diderot, Paris, France. cecile.julier@inserm.fr
Abstract Wolcott-Rallison syndrome (WRS) is a rare autosomal recessive disease, characterized by neonatal/early-onset non-autoimmune insulin-requiring diabetes associated with skeletal dysplasia and growth retardation. Fewer than 60 cases have been described in the literature, although WRS is now recognised as the most frequent cause of neonatal/early-onset diabetes in patients with consanguineous parents. Typically, diabetes occurs before six months of age, and skeletal dysplasia is diagnosed within the first year or two of life. Other manifestations vary between patients in their nature and severity and include frequent episodes of acute liver failure, renal dysfunction, exocrine pancreas insufficiency, intellectual deficit, hypothyroidism, neutropenia and recurrent infections. Bone fractures may be frequent. WRS is caused by mutations in the gene encoding eukaryotic translation initiation factor 2α kinase 3 (EIF2AK3), also known as PKR-like endoplasmic reticulum kinase (PERK). PERK is an endoplasmic reticulum (ER) transmembrane protein, which plays a key role in translation control during the unfolded protein response. ER dysfunction is central to the disease processes. The disease variability appears to be independent of the nature of the EIF2AK3 mutations, with the possible exception of an older age at onset; other factors may include other genes, exposure to environmental factors and disease management. WRS should be suspected in any infant who presents with permanent neonatal diabetes associated with skeletal dysplasia and/or episodes of acute liver failure. Molecular genetic testing confirms the diagnosis. Early diagnosis is recommended, in order to ensure rapid intervention for episodes of hepatic failure, which is the most life threatening complication. WRS should be differentiated from other forms of neonatal/early-onset insulin-dependent diabetes based on clinical presentation and genetic testing. Genetic counselling and antenatal diagnosis is recommended for parents of a WRS patient with confirmed EIF2AK3 mutation. Close therapeutic monitoring of diabetes and treatment with an insulin pump are recommended because of the risk of acute episodes of hypoglycaemia and ketoacidosis. Interventions under general anaesthesia increase the risk of acute aggravation, because of the toxicity of anaesthetics, and should be avoided. Prognosis is poor and most patients die at a young age. Intervention strategies targeting ER dysfunction provide hope for future therapy and prevention.
PMID: 21050479
2009
Remodelling sympathetic innervation in rat pancreatic islets ontogeny
Cabrera-Vásquez S, Navarro-Tableros V, Sánchez-Soto C, Gutiérrez-Ospina G, Hiriart M. BMC Dev Biol. 2009 Jun 17;9:34. PMID: 19534767
http://www.ncbi.nlm.nih.gov/pubmed/19534767
- "Adult pancreatic β cells secrete insulin in response to an increase in extracellular glucose. At birth, this response is not fully developed as neonate β-cells are insensitive to glucose and synthesize and secrete less insulin than adults [1]. Pancreatic islets are innervated by autonomic fibres. In particular, sympathetic neural cell bodies are located in the superior mesenteric and celiac ganglia and are components of the splanchnic nerve and parasympathetic innervation comes from the vagus nerve [2]."
Conclusion The results suggest that NGF signalling play an important role in the guidance of blood vessels and sympathetic fibres toward the islets during foetal and neonatal stages and could also preserve innervation at later stages of life.
1. Navarro-Tableros V, Fiordelisio T, Hernandez-Cruz A, Hiriart M: Physiological development of insulin secretion, calcium channels, and GLUT2 expression of pancreatic rat beta-cells.
Am J Physiol Endocrinol Metab 2007, 292(4):E1018-1029.
2. Salvioli B, Bovara M, Barbara G, De Ponti F, Stanghellini V, Tonini M, Guerrini S, Cremon C, Degli Esposti M, Koumandou M, et al.: Neurology and neuropathology of the pancreatic innervation. Jop 2002, 3(2):26-33
Islet architecture: A comparative study
Islets. 2009 Sep-Oct;1(2):129-36.
Kim A, Miller K, Jo J, Kilimnik G, Wojcik P, Hara M. Source Department of Medicine, The University of Chicago, Chicago, IL, USA.
Abstract
Emerging reports on the organization of the different hormone-secreting cell types (alpha, glucagon; beta, insulin; and delta, somatostatin) in human islets have emphasized the distinct differences between human and mouse islets, raising questions about the relevance of studies of mouse islets to human islet physiology. Here, we examine the differences and similarities between the architecture of human and mouse islets. We studied islets from various mouse models including ob/ob and db/db and pregnant mice. We also examined the islets of monkeys, pigs, rabbits and birds for further comparisons. Despite differences in overall body and pancreas size as well as total beta-cell mass among these species, the distribution of their islet sizes closely overlaps, except in the bird pancreas in which the delta-cell population predominates (both in singlets and clusters) along with a small number of islets. Markedly large islets (>10,000 mum(2)) were observed in human and monkey islets as well as in islets from ob/ob and pregnant mice. The fraction of alpha-, beta- and delta-cells within an islet varied between islets in all the species examined. Furthermore, there was variability in the distribution of alpha- and delta-cells within the same species. In summary, human and mouse islets share common architectural features that may reflect demand for insulin. Comparative studies of islet architecture may lead to a better understanding of islet development and function.
PMID: 20606719
Islet size and β-cell ratio for different species
| Species | Islet size | β-cell ratio |
| Human | 50 ± 29 | 0.64 ± 0.21 |
| Monkey | 67 ± 38* | 0.79 ± 0.14* |
| Pig | 49 ± 15a | 0.89 ± 0.11* |
| Rabbit | 64 ± 28* | 0.79 ± 0.17* |
| Bird | 24 ± 6* | 0.46 ± 0.24* |
| Wild-type mouse | 116 ± 80* | 0.85 ± 0.14* |
| ob/ob mouse | 86 ± 76* | 0.92 ± 0.11* |
| db/db mouse | 47 ± 24b | 0.53 ± 0.24c |
| Pregnant mouse | 112 ± 94* | 0.84 ± 0.22* |
*p < 0.0001 compared with human. ap = 0.65 bp = 0.42
cp = 0.0004
Islet size is described as an effective diameter of a circle, which depicts the same area as a measured islet area. β-cell ratio is the area ratio of β-cells in an islet. Both data sets are expressed as the mean value with its standard deviation.
