Gastroenteropancreatic Regulatory Peptide Structures: An Overview
Edwin E. Daniel in Neuropeptide Function in the Gastrointestinal Tract, 2019
Ingestion of protein or lipids elicits large rises in plasma PP levels, whereas carbohydrate ingestion results in relatively small elevations. These postprandial elevations of plasma PP occur in a biphasic manner; the cephalic-phase plasma PP response occurs rapidly and is totally abolished by truncal vagotomy. The secondary or GI phase of PP release occurs later and may be mediated by enteropancreatic reflexes connecting the gut and pancreas and by humoral mechanisms. Although no clear physiological role for PP has yet been established, administration of PP in doses that result in plasma levels approximating those seen in the postprandial state produces inhibition of pancreatic exocrine secretion and biliary tract motility. The functional aspects of PP have been reviewed recently.181 In summary, pancreatic polypeptide, contained in specific cells in the endocrine pancreas, appears to exert its activity in a classical hormonal fashion.
Carcinoid tumors
Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner in Endocrine Surgery, 2017
NSE is another biochemical marker that has been investigated for its use in detecting NETs. While the specificity of NSE in one study was 100%, the sensitivity was quite low at 32.9% [19]. Foregut tumors are unique in that they secrete mostly histamine. The urine metabolite of histamine is methyl-imidazole acetic acid, which can be measured. Pancreatic polypeptide, produced primarily in the islet cells of the pancreas, can also be produced by pancreatic NETs and some gastrointestinal NETs. In one study, it was elevated in 13% of patients with carcinoid tumors. Additional research is necessary in order to establish the significance of this marker. In the same study, gastrin was only elevated in 3% of patients with carcinoid tumors. While it is useful in the detection of other NETs, its use in the detection of carcinoid tumors remains limited [20].
The gastrointestinal tract
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
Cells that synthesize gut peptides are scattered throughout the length of the gastrointestinal tract, although the secretory cells are often concentrated in one segment of the tract. Many of these peptides are present in other organs, particularly the brain, where they probably act as neurotransmitters. Gastrin is released from the gastrin-secreting G cells in the gastric antrum in response to distension and to protein. It stimulates the contraction of the stomach muscles and the secretion of gastric acid. Acid inhibits gastrin release by negative feedback.Cholecystokinin stimulates contraction of the gall bladder and the release of pancreatic digestive enzymes.Secretin stimulates the release of pancreatic fluid rich in bicarbonate.Pancreatic polypeptide inhibits pancreatic secretion.Vasoactive intestinal polypeptide (VIP) and motilin regulate gut motility.
Metabolic response to oral glucose tolerance test performed in neutral and warm environmental temperature
Published in International Journal of Hyperthermia, 2019
Sophie Antoine-Jonville, Dalia El Khoury, Cécile Faure, Keyne Charlot, Olivier Hue, Marie-Dominique Hardy-Dessources
Another factor that may help explain our results is the gastrointestinal contribution to glucose homeostasis. An increased absorption rate with a lower proportion of the glucose load retained by the splanchnic bed could lead to higher peak values of blood glucose. We assumed that the measurement of the pancreatic polypeptide hormone would affirm or reject this hypothesis. PP is known to play a role in the regulation of pancreatic endocrine secretions and other metabolic processes. For example, PP infusion reverses hepatic insulin resistance in patients who are PP-deficient due to pancreatic resection or chronic pancreatitis [28]. It is expected to increase rapidly in healthy humans after food ingestion, particularly when the meal is rich in proteins, although its actions are quite complex since intravenous boluses and oral intake loads have opposite effects [29]. Its interaction with glucose metabolism and insulin sensitivity, in association with its effects on gut function, suggest it may be a serious candidate. However, we were unable to identify the effects of the environmental temperature, the glucose load, or the interaction between them. Our understanding was thus not improved by the PP results in this study.
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].
Hnf1b-CreER causes efficient recombination of a Rosa26-RFP reporter in duct and islet δ cells
Published in Islets, 2021
Meritxell Rovira, Miguel Angel Maestro, Vanessa Grau, Jorge Ferrer
Our original studies focused on labeling of β and α cells because they are by far the most prevalent islet endocrine cells, and because those studies needed to ensure if the model was valid for testing the hypothesis that duct cells give rise to β cells. Analysis of tamoxifen-treated Hnf1b-CreERT2; Rosa26-RFP mice, however, revealed conspicuous RFP+ cells in the mantle of some pancreatic islets, and were glucagon/insulin-negative, which led us to examine other hormones. Somatostatin-expressing δ cells make up 1–5% of islet endocrine cells.16 We found that on average 49.5% ± 4.1 of δ cells were RFP+ in Hnf1b-CreERT2; Rosa26-RFP islets (see Figure 1(c), showing an islet with multiple δ cells, and quantifications in Figure 1(e)). By contrast, only 1.45% ± 0.6 of pancreatic polypeptide cells were RFP+ (Figure 1(d,e)).
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