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Animal Models of Genetic Obesity: Peripheral Tissue Changes
Published in Claude Bouchard, The Genetics of Obesity, 2020
Patricia R. Johnson, Francine Gregoire
Pancreatic polypeptide (PP) levels have also been reported to be normal, elevated, and depressed in obese subjects, but the majority of the data obtained in humans reveal normal values for PP and somatostatin.111 Somatostatin is a potent inhibitor of pancreatic insulin release, and a potential role for somatostatin in the pathogenesis of hyperinsulinemia has been suggested.112 In ob/ob mice, lower than normal concentrations were reported for both the pancreas and the stomach.113 By contrast, in obese Zucker and obese SHR/N-cp rats, pancreatic levels of somatostatin were significantly higher than those seen in lean littermates. Gastric somatostatin levels were reduced, but only in obese Zucker rats.112
Digestive and Metabolic Actions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The insulin-secreting beta cells, which make up 70%–80% of the islet cells, have all the components necessary for DA synthesis, secretion, and action. Insulin is primarily released in response to elevated blood glucose levels, and its actions are fundamental to the maintenance of glucose homeostasis [60]. Binding to its glycoprotein receptor, insulin is the only hormone that lowers blood glucose levels by promoting glucose uptake by the various cells. The opposite effects (i.e., glycogenolysis and gluconeogenesis) are partly under the control of glucagon. The role of the pancreatic polypeptide in metabolism is unclear except that it serves as a satiety hormone. The main effect of somatostatin on metabolism is via its inhibition of GH, a major metabolic hormone.
The Endocrine Pancreas
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Pancreatic polypeptide is secreted as a 36-amino acid peptide from the PP cells within the islet as well as from cells scattered throughout the exocrine pancreas and in the gut. Pancreatic polypeptide seems to inhibit gallbladder contraction, pancreatic enzyme production, and gastric acid secretion. However, its effects in these regards are weak and of unclear physiologic significance. Pancreatic polypeptide seems to be largely released in response to cholinergic innervation in response to meals, and hypoglycemia and high serum levels are attained. Pancreatic polypeptide-secreting tumors are associated with no metabolic or other abnormalities except for occasional rash and diarrhea.45
Post-pancreatitis diabetes mellitus: insight on optimal management with nutrition and lifestyle approaches
Published in Annals of Medicine, 2022
Amandeep Singh, Manik Aggarwal, Rajat Garg, Tyler Stevens, Prabhleen Chahal
Pancreatic inflammation leads to structural and functional loss of islet cell mass leading to loss of insulin, glucagon, and pancreatic polypeptide, which leads to the development of difficult to control diabetes with large fluctuations in blood glucose, which are difficult to control. In addition to the loss of glucagon response to hypoglycaemia, poor eating patterns due to pain and nausea, carbohydrate malabsorption, and alcohol use can also lead to labile blood glucose levels. A significant proportion of these patients also have concomitant EPI, leading to fat malabsorption with loss of fat-soluble vitamins. Loss of vitamin D can lead to metabolic bone disease and osteoporosis. The lack of luminal enzymes may also decrease the incretin response, further impairing glycemic control [37]. The management of PPDM is challenging and could be exhaustive for general practitioners taking care of these patients. Besides routine diabetic care including monitoring for nephropathy, retinopathy, and neuropathy they have to take care of pancreatitis-related complications including post-pancreatitis pain, poor oral intake, psychological issues, EPI, and vitamin and mineral deficiencies.
Vesiculin derived from IGF-II drives increased islet cell mass in a mouse model of pre-diabetes
Published in Islets, 2022
Kate L. Lee, Jacqueline F. Aitken, Xun Li, Kirsten Montgomery, Huai-L. Hsu, Geoffrey M. Williams, Margaret A. Brimble, Garth J.S. Cooper
At the end of the 8 weeks, organ weights did not indicate any difference for pancreas, heart, kidney and liver (Table 1B). Histological analysis of the pancreas was performed on three representative animals per group. A total of 147 sections were analyzed. In total, 424 individual islets were analyzed on 49 sections co-stained for insulin and glucagon, 457 individual islets were analyzed on 49 sections co-stained insulin and PP, and 477 individual islets were analyzed on 49 sections co-stained for insulin and somatostatin. Immunofluorescent labeling of islet hormones revealed larger proportions of both insulin and glucagon staining per section area in the vesiculin-treated hemizygous hA-tg mice (Figure 4A and B). By contrast, there were no significant differences in pancreatic polypeptide or somatostatin (Figure 4C and D). Section area per islet indicated that the vesiculin-treated non-tg group had the lowest number of islets but this finding may have been driven by some sections from one individual which contained no discernible islet tissue. There was no difference between the other groups (Figure 4E).
Changes in colonic enteroendocrine cells of patients with irritable bowel syndrome following fecal microbiota transplantation
Published in Scandinavian Journal of Gastroenterology, 2022
Tarek Mazzawi, Trygve Hausken, Magdy El-Salhy
Patients with IBS have altered densities of enteroendocrine cells throughout the GI tract [10,24–27] that tend to change following manipulations of diet [7,11,28–32] and of the gut microbiota [20,21]. Previous publication shows that dietary manipulation also affects the gut microbiota [33]. The dynamic changes that occur to the enteroendocrine cells following their interactions with the surrounding stimuli stimulate their release of the gut hormones to regulate the different functions of the GI tract [5,34]. Chromogranin A is a common marker for the enteroendocrine cells [35–38]. Serotonin modulates the GI visceral sensitivity [24,39–42] stimulates large intestinal motility, and accelerates intestinal transit time [39–47]. Somatostatin inhibits intestinal contraction [34,48], and stimulates the absorption of water and electrolytes [34]. PYY stimulates the absorption of water and electrolytes and is a major regulator of the ‘ileal brake’ [24,49]. Enteroglucagon (oxyntomodulin) inhibits gastric and pancreatic secretions and reduces gastric motility [48]. Pancreatic polypeptide inhibits pancreatic secretion; relaxes gall bladder; and stimulates motility of stomach and small intestine [48].