Impact of intestinal electrical stimulation on nutrient‐induced GLP‐1 secretion in vivo

Background Increases in L‐cell release of GLP‐1 are proposed to serve as a negative feedback signal for postprandial changes in gastric emptying and/or motility. Previous ex vivo data suggests that direct electrical stimulation (E‐stim) of ileal segments stimulates secretion of GLP‐1. This suggests...

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Published inNeurogastroenterology and motility Vol. 25; no. 8; pp. 700 - e513
Main Authors Sandoval, D., Dunki‐Jacobs, A., Sorrell, J., Seeley, R. J., D'Alessio, D. D.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.08.2013
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Summary:Background Increases in L‐cell release of GLP‐1 are proposed to serve as a negative feedback signal for postprandial changes in gastric emptying and/or motility. Previous ex vivo data suggests that direct electrical stimulation (E‐stim) of ileal segments stimulates secretion of GLP‐1. This suggests potential feed‐forward increases in GLP‐1 driven by intestinal neuronal and/or motor activity. Methods To determine if E‐stim could increase GLP‐1 levels in an in vivo setting, we administered E‐stim and nutrients to male Long‐ Evans rats (300–350 g) under general anesthesia. Key Results Nutrient infusion into the duodenum or ileum significantly increased plasma GLP‐1 levels, but E‐stim applied to these locations did not (P < 0.05). However, the combination of E‐stim and nutrient infusion, in either the ileum or duodenum, significantly increased plasma GLP‐1 when compared to nutrient infusion alone (P < 0.05), and this effect was not blocked by either norepinephrine or atropine. To test the impact of intestinal motor activity, the effect of extra‐luminal mechanical stimulation (M‐stim) on GLP‐1 levels was assessed. In the duodenum, but not the ileum, M‐stim plus nutrient infusion significantly increased GLP‐1 over nutrient infusion or M‐stim alone (P < 0.05). Conclu‐sions & Inferences Thus, both E‐ and M‐stim of the duodenum, but only E‐stim of the ileum augmented nutrient‐stimulated GLP‐1 release. These data demonstrate that factors beyond enteral nutrients could contribute to the regulation of GLP‐1 secretion.
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ISSN:1350-1925
1365-2982
DOI:10.1111/nmo.12152