PMID: 9436865Jan 22, 1998Paper

The ethanol augmentation of glucose-induced insulin secretion is abolished by calcium antagonism with nifedipine: no evidence for a role of glucagon-like peptide-1 (GLP-1)

Pancreas
J SvartbergN Adner

Abstract

We studied the effect of ethanol and calcium antagonism (nifedipine) on insulin- (n = 8) and glucagon-like peptide-1 (GLP-1) (n = 6) secretion in healthy subjects. Four experiments in random order were performed (control, ethanol, nifedipine, and combination). Intravenous glucose tolerance tests were performed with and without pretreatment with oral ethanol and nifedipine. Ethanol pretreatment was followed by increased insulin (ethanol vs. control; p < 0.01) and C-peptide (ethanol vs. control; p < 0.05) areas after intravenous glucose (0-20 min), indicating that ethanol augments insulin secretion. Calcium antagonism with nifedipine abolished the ethanol augmentation of insulin secretion (insulin area 0-20 min, ethanol vs. combination, p < 0.05; and C-peptide area 0-20 min, ethanol vs. combination, p < 0.01). The GLP-1 response (area 0-90 min) was not significantly affected by ethanol.

Related Concepts

Related Feeds

Cardiovascular Biology of GLP-1

Glucagon-like peptide 1 (GLP-1) plays a role in glucose metabolism, energy homeostasis, and inflammation suppression. GLP-1 receptor signaling has been shown to impact cardiovascular function. This feed focuses on the role of GLP-1 and GLP-1 receptor agonists on cardiovascular biology.