-An-inverse-correlation-between-FFA-and-GLP1-concentrations-existed-in-both-trials-b

In rat intestine, acipimox did not affect GLP-1 secretion, and l-cells did not consistently express the putative CONCLUSIONS: Acipimox treatment increases systemic GLP-1 levels in both obese subjects and hypopituitary patients. Our in vitro data indicate that the Conflict of interest statement: Disclosure statement: The authors of this work declare no potential conflicts of interest relevant to this article.Ileal release of glucagon-like peptide-1 (GLP-1). Association with inhibition of There is evidence that the distal intestine participates in the regulation of gastric motor and secretory function. It was the aim of this study to examine in greater detail the effects of ileal nutrient exposure on human gastric acid secretion and to investigate potential intermediary mechanisms. Twelve normal subjects were intubated with an oroileal multilumen tube assembly for gastric, duodenal, and ileal perfusion of marker and test solutions, aspiration, and intestinal manometry.

semaglutide studied ileal effects on gastric acid output in the unstimulated, interdigestive state (during early phase II, N = 6), and during endogenous stimulation by intraduodenal essential amino acid perfusion, N = 6) and on release of candidate humoral mediators, peptide YY (PYY) and glucagonlike peptide-1 (GLP-1), both known inhibitors of human gastric acid secretion. Compared with ileal saline perfusion, ileal carbohydrate (total caloric load: 60 kcal) decreased interdigestive gastric acid output by 64% (P < 01), and endogenously stimulated output by 68%, respectively (P < 005). Under all experimental conditions, ileal carbohydrate increased plasma GLP-1 by 80-100% (all P < 005). Ileal lipid perfusion had similar inhibitory effects on gastric acid output and stimulatory effects on GLP-1 release as had ileal carbohydrate. By contrast, ileal perfusion with peptone had no or only weak effects on either acid output or plasma GLP-1. Plasma PYY concentrations and suppression of gastric secretion in response to ileal perfusions were not correlated. In humans, both interdigestive and endogenously stimulated gastric acid output are inhibited in response to intraileal carbohydrate or lipids, but not protein.

(ABSTRACT TRUNCATED AT 250 WORDS)Vasorelaxant effect of glucagon-like peptide-(7-36)amide and amylin on the The gastrointestinal peptides glucagon-like peptide-1(7-36)amide (GLP-1) and amylin are currently being tested in clinical trials for the treatment of diabetes mellitus due to their effects in lowering blood glucose. Receptors for these polypeptides also exist in the lung and since polypeptides are known to modulate airway and pulmonary vascular tone, we investigated whether GLP-1 and amylin act similarly in the lung. We compared their effects with the well-known actions of calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP). Both GLP-1 and amylin induced a dose-dependent and time-reversible endothelial-dependent relaxation of preconstricted pulmonary artery rings. Amylin was approximately as strong as VIP and CGRP, GLP-1 however, was 2-fold less potent. GLP-1 as well as amylin also reduced the vascular tone in the isolated, perfused and ventilated rat lung. In contrast to their action on the pulmonary vasculature, neither GLP-1 nor amylin showed any effect on the tone of isolated preconstricted trachea rings.

In conclusion, GLP-1 and amylin represent two additional peptides which may modulate pulmonary vascular tone.The ethanol augmentation of glucose-induced insulin secretion is abolished by calcium antagonism with nifedipine: no evidence for a role of glucagon-like We studied the effect of ethanol and calcium antagonism (nifedipine) on insulin- (n = 8) and glucagon-like peptide-1 (GLP-1) (n = 6) secretion in healthy subjects. Four experiments in random order were performed (control, ethanol, nifedipine, and combination). API Hormones and Regulation were performed with and without pretreatment with oral ethanol and nifedipine. Ethanol pretreatment was followed by increased insulin (ethanol vs. control; p < 01) and C-peptide (ethanol vs. control; p < 05) areas after intravenous glucose (0-20 min), indicating that ethanol augments insulin secretion.

Calcium antagonism with nifedipine abolished the ethanol augmentation of insulin secretion (insulin area 0-20 min, ethanol vs. combination, p < 05; and C-peptide area 0-20 min, ethanol vs. combination, p < 01). The GLP-1 response (area 0-90 min) was not significantly affected by ethanol.Therapeutic strategies based on glucagon-like peptide 1.Glucagon-like peptide (GLP)-1 is an incretin hormone with potent glucose-dependent insulinotropic and glucagonostatic actions, trophic effects on the pancreatic beta-cells, and inhibitory effects on gastrointestinal secretion and motility, which combine to lower plasma glucose and reduce glycemic excursions. Furthermore, via its ability to enhance satiety, GLP-1 reduces food intake, thereby limiting weight gain, and may even cause weight loss.