Regulation of gut hormone secretion. Studies using isolated perfused intestines.

Research output: Contribution to journalReviewResearchpeer-review

A review. The incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted from enteroendocrine cells in the intestine along with other gut hormones (PYY, CCK and neurotensin) shown to affect metab. and/or appetite. The secretion of many gut hormones is highly increased after gastric bypass operations, which have turned out to be an effective therapy of not only obesity but also type 2 diabetes. These effects are likely to be due, at least in part, to increases in the secretion of these gut hormones (except GIP). Therefore, stimulation of the endogenous hormone represents an appealing therapeutic strategy, which has spurred an interest in understanding the regulation of gut hormone secretion and a search for particularly GLP-1 and PYY secretagogues. The secretion of the gut hormones is stimulated by oral intake of nutrients often including carbohydrate, protein and lipid. This review focuses on stimulators of gut hormone secretion, the mechanisms involved, and in particular models used to investigate secretion. A major break-through in this field was the development of methods to identify and isolate specific hormone producing cells, which allow detailed mapping of the expression profiles of these cells, whereas they are less suitable for physiol. studies of secretion. Isolated perfused prepns. of mouse and rat intestines have proven to be reliable models for dynamic hormone secretion and should be able to bridge the gap between the mol. details derived from the single cells to the integrated patterns obsd. in the intact animals. [on SciFinder(R)]
Original languageEnglish
JournalPeptides
Volume77
Pages (from-to)47-53
Number of pages7
ISSN0196-9781
DOIs
Publication statusPublished - Mar 2016

Bibliographical note

M1 - Copyright (C) 2015 American Chemical Society (ACS). All Rights Reserved.

CAPLUS AN 2015:1337275(Journal; General Review)

ID: 150700961