Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal.
- 1 May 1994
- journal article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 93 (5), 2263-2266
- https://doi.org/10.1172/jci117225
Abstract
Glucagon-like peptide 1 [7-36 amide] (GLP-1) has been shown to enhance insulin secretion in healthy and type II diabetic humans, and to increase glucose disposal in type I diabetic patients. To further define its action on glucose kinetics, we studied six healthy subjects who received either GLP-1 (45 pmol/kg per h) or 150 mM saline on two mornings during which a modified intravenous glucose tolerance test was performed. Plasma insulin and glucose levels were analyzed using Bergman's minimal model of glucose kinetics to derive indices of insulin sensitivity (SI) and glucose effectiveness at basal insulin (SG), the latter a measure of glucose disposition independent of changes in insulin. In addition, basal insulin concentrations, the acute insulin response to glucose (AIRg), plasma glucagon levels, and the glucose disappearance constant (Kg) were measured on the days that subjects received GLP-1 or saline. Compared with saline infusions, GLP-1 increased the mean Kg from 1.61 +/- 0.20 to 2.65 +/- 0.25%/min (P = 0.022). The enhanced glucose disappearance seen with GLP-1 was in part the result of its insulinotropic effect, as indicated by a rise in AIRg from 240 +/- 48 to 400 +/- 78 pM (P = 0.013). However, there was also an increase in SG from 1.77 +/- 0.11 to 2.65 +/- 0.33 x 10(-2).min-1 (P = 0.038), which was accounted for primarily by insulin-independent processes, viz glucose effectiveness in the absence of insulin. There was no significant effect of GLP-1 on SI or basal insulin, and glucagon levels were not different during the glucose tolerance tests with or without GLP-1. Thus, GLP-1 improves glucose tolerance both through its insulinotropic action and by increasing glucose effectiveness. These findings suggest that GLP-1 has direct effects on tissues involved in glucose disposition. Furthermore, this peptide may be useful for studying the process of insulin-independent glucose disposal, and pharmacologic analogues may be beneficial for treating patients with diabetes mellitus.This publication has 22 references indexed in Scilit:
- Minimal Model Analysis of Intravenous Glucose Tolerance Test-Derived Insulin Sensitivity in Diabetic Subjects*Journal of Clinical Endocrinology & Metabolism, 1990
- Treatment with a Somatostatin Analog Decreases Pancreatic B-Cell and Whole Body Sensitivity to Glucose*Journal of Clinical Endocrinology & Metabolism, 1990
- Glucagon and the Glucagon-like PeptidesPancreas, 1990
- A Modified Protocol for Estimation of Insulin Sensitivity with the Minimal Model of Glucose Kinetics in Patients with Insulin-Dependent Diabetes*Journal of Clinical Endocrinology & Metabolism, 1990
- Toward Physiological Understanding of Glucose Tolerance: Minimal-Model ApproachDiabetes, 1989
- Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humansAmerican Journal of Physiology-Endocrinology and Metabolism, 1988
- The Insulin Sensitivity Index in Nondiabetic Man: Correlation Between Clamp-derived and IVGTT-derived ValuesDiabetes, 1986
- Importance of Glucose Per Se to Intravenous Glucose Tolerance: Comparison of the Minimal-Model Prediction with Direct MeasurementsDiabetes, 1985
- Quantitative estimation of insulin sensitivity.American Journal of Physiology-Endocrinology and Metabolism, 1979
- HYPERGLYCEMIA PER SE (INSULIN AND GLUCAGON WITHDRAWN) CAN INHIBIT HEPATIC GLUCOSE PRODUCTION IN MANJournal of Clinical Endocrinology & Metabolism, 1979