Glucagon‐like peptide‐2 mobilizes lipids from the intestine by a systemic nitric oxide‐independent mechanism. Issue 11 (19th August 2019)

• Record Type: Journal Article
• Authors: Xiao, Changting; Stahel, Priska; Morgantini, Cecilia; Nahmias, Avital; Dash, Satya; Lewis, Gary F.
• Is Part Of: Diabetes, obesity & metabolism. Volume 21:Issue 11(2019)
• Page Start: 2535
• Page End: 2541
• Publication Date: 2019-08-19
• Subjects: clinical physiology -- dyslipidaemia; Diabetes -- Periodicals; Obesity -- Periodicals; Metabolism -- Disorders -- Periodicals; Clinical pharmacology -- Periodicals; 616.462
• DOI: 10.1111/dom.13839
• Languages: English
• ISSNs: 1462-8902

Abstract

Abstract: Aim: To test the hypothesis that gut hormone glucagon‐like peptide‐2 (GLP‐2) mobilizes intestinal triglyceride (TG) stores and stimulates chylomicron secretion by a nitric oxide (NO)‐dependent mechanism in humans. Methods: In a randomized, single‐blind, cross‐over study, 10 healthy male volunteers ingested a high‐fat formula followed, 7 hours later, by one of three treatments: NO synthase inhibitor L‐N G ‐monomethyl arginine acetate (L‐NMMA) + GLP‐2 analogue teduglutide, normal saline + teduglutide, or L‐NMMA + placebo. TG in plasma and lipoprotein fractions were measured, along with measurement of blood flow in superior mesenteric and coeliac arteries using Doppler ultrasound in six participants. Results: Teduglutide rapidly increased mesenteric blood flow and TG concentrations in plasma, in TG‐rich lipoproteins, and most robustly in chylomicrons. L‐NMMA significantly attenuated teduglutide‐induced enhancement of mesenteric blood flow but not TG mobilization and chylomicron secretion. Conclusions: GLP‐2 mobilization of TG stores and stimulation of chylomicron secretion from the small intestine appears to be independent of systemic NO in humans.