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|Title:||Effects of intravenous glucagon-like peptide-1 on gastric emptying and intragastric distribution in healthy subjects: Relationships with postprandial glycemic and insulinemic responses|
|Citation:||Journal of Clinical Endocrinology and Metabolism, 2006; 91(5):1916-1923|
|Tanya J. Little, Amelia N. Pilichiewicz, Antonietta Russo, Liza Phillips, Karen L. Jones, Michael A. Nauck, Judith Wishart, Michael Horowitz and Christine Feinle-Bisset|
|Abstract:||Context: The inhibitory action of glucagon-like peptide-1 (GLP-1) on gastric emptying (GE) is likely to be important in mediating its effects on postprandial glycemia, appetite, and gastrointestinal symptoms. Objective: The objective of the study was to evaluate the effects of "low" and "high" doses of iv GLP-1 on GE, intragastric meal distribution, glycemia, insulinemia, and appetite. Design: Ten healthy males were studied on 3 d. GE of a solid (ground beef)/liquid (glucose) meal, blood glucose, plasma insulin, glucagon and glucose-dependent insulinotropic peptide, appetite perceptions, and gastrointestinal symptoms were evaluated during iv infusion of: 1) GLP-1 at 0.3 pmol·kg–1·min–1 (GLP-1 0.3); 2) GLP-1 at 0.9 pmol·kg–1·min–1 (GLP-1 0.9); and 3) 0.9% saline. Results: GLP-1 0.3 and 0.9 slowed GE of solid (intragastric retention at t = 100 min; saline: 28 ± 5%; GLP-1 0.3: 53 ± 6%; GLP-1 0.9: 58 ± 7%; P < 0.001) and liquid (time for 50% of the liquid to empty, saline: 28 ± 2 min; GLP-1 0.3: 42 ± 7 min; GLP-1 0.9: 50 ± 9 min; P < 0.001). Both doses of GLP-1 induced gastroparesis in about half the cohort and increased meal retention in the distal stomach (P < 0.05). GLP-1 attenuated the rises in glucose, insulin, and glucose-dependent insulinotropic peptide (P < 0.05). There was an inverse relationship between blood glucose at t = 15 min and the time for 50% of the liquid to empty (r = –0.70, P < 0.001). Conclusions: In healthy subjects exogenous GLP-1 increases meal retention in the distal stomach and, even when administered in a "low" dose, frequently induces "gastroparesis," and the effects of GLP-1 on postprandial glycemia are predictable on the basis of its effect on GE, supporting the concept that GE is a major target mechanism for the clinical use of incretin mimetics.|
|Keywords:||Stomach; Humans; Gastric Inhibitory Polypeptide; Glucagon; Insulin; Blood Glucose; Treatment Outcome; Injections, Intravenous; Hunger; Appetite; Satiety Response; Gastric Emptying; Postprandial Period; Adult; Male; Glucagon-Like Peptide 1|
|Description:||Copyright © 2006 by The Endocrine Society|
|Appears in Collections:||Medicine publications|
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