Glucagon-like peptide 1 abolishes the postprandial rise in triglyceride concentrations and lowers levels of non-esterified fatty acids in humans.
Meier, J. J. 1,4; Gethmann, A. 1; Gotze, O. 1; Gallwitz, B. 1; Holst, J. J. 2; Schmidt, W. E. 1; Nauck, M. A. 3
[Article]
Diabetologia.
49(3):452-458, March 2006.
(Format: HTML, PDF)
Aims/hypothesis: Diabetic dyslipidaemia contributes to the excess morbidity and mortality in patients with type 2 diabetes. Exogenous glucagon-like peptide 1 (GLP-1) lowers postprandial glycaemia predominantly by slowing gastric emptying. Therefore, the effects of GLP-1 on postprandial lipid levels and gastric emptying were assessed.
Methods: 14 healthy male volunteers were studied with an i.v. infusion of GLP-1 (1.2 pmol kg-1 min-1) or placebo over 390 min in the fasting state. A solid test meal was served and gastric emptying was determined using a 13C-labelled sodium octanoate breath test. Venous blood was drawn frequently for measurement of glucose, insulin, C-peptide, glucagon, GLP-1, triglycerides and NEFA.
Results: GLP-1 administration lowered fasting and postprandial glycaemia (p<0.0001). Gastric emptying was delayed by GLP-1 compared with placebo (p<0.0001). During GLP-1 administration, insulin secretory responses were higher in the fasting state but lower after meal ingestion. After meal ingestion, triglyceride plasma levels increased by 0.33 /-0.14 mmol/l in the placebo experiments (p<0.0001). In contrast, the postprandial increase in triglyceride levels was completely abolished by GLP-1 (change in triglycerides, -0.023 /-0.045 mmol/l; p<0.05). During GLP-1 infusion, plasma concentrations of NEFA were suppressed by 39% in the fasting state (p<0.01) and by 31 /-5% after meal ingestion (p<0.01).
Conclusions/interpretation: GLP-1 improves postprandial lipidaemia, presumably as a result of delayed gastric emptying and insulin-mediated inhibition of lipolysis. Thus, by lowering both glucose and lipid concentrations, GLP-1 administration may reduce the cardiovascular risk in patients with type 2 diabetes.
(C) 2006 Springer. Part of Springer Science Business Media