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Classic notions of GLP-1 acting as a meal-stimulated hormone from the distal gut are challenged by data supporting production of GLP-1 in the endocrine pancreas, and by the importance of
.Short-chain fatty acids stimulate the secretion of endogenous GLP-1 from L cells that accelerates colonic peristalsis. Thus, besides the well-known humoral insulinotropic
.GLP-1 receptor agonists (GLP-1RAs) can reduce blood glucose levels and have been reported to have several extrapancreatic effects [3]. GLP-1 suppresses gastric emptying
.Explore how the precise GLP-1 sequence orchestrates vital bodily processes and its pivotal role in advancing health and medicine.
.There is now considerable attention, including in the public media, on the effect of both long-acting and short-acting GLP-1RAs to delay gastric emptying.
In summary, GLP-1 agonists and analogs are integral to the management of patients with type 2 diabetes mellitus and obesity, and their effects are mediated, at least in part, by retardation of
Further research is needed to gain a better understanding of the actions of GLP-1 and incretin-based therapies on small bowel motility, the extent of the role of endogenous GLP-1 on gut
.In this review, we summarize the effects of GLP-1 and incretin-based therapeutics on gastric, biliary and small intestinal function. An improved understanding of
Because GLP-1 accelerates peristalsis in the proximal colon, the present study aimed to explore whether LPS facilitates colonic peristalsis by stimulating L cell-derived GLP-1 release.
GLP-1 is secreted from L cells in the small intestine and colon through post-translational processing of proglucagon (which also gives rise to GLP-2 – a trophic factor for intestinal
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