Open AccessDifferential Effects of Glucagon-like Peptide-1 (7-36)Amide Versus Cholecystokinin on Arginine-Induced Islet Hormone Release In Vivo and In Vitro
Author(s) -
Amel Guenifi,
Bo Åhrén,
Samy M. AbdelHalim
Publication year - 2001
Publication title -
pancreas
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.061
H-Index - 104
eISSN - 1536-4828
pISSN - 0885-3177
DOI - 10.1097/00006676-200101000-00010
Subject(s) - medicine , endocrinology , arginine , somatostatin , glucagon , in vivo , insulin , cholecystokinin , islet , chemistry , incretin , pancreas , glucagon like peptide 1 , hormone , biology , biochemistry , amino acid , diabetes mellitus , receptor , type 2 diabetes , microbiology and biotechnology
We compared the effects of two incretin hormones, glucagon-like peptide-1 (7-36)amide (GLP-1) and cholecystokinin (CCK), on islet hormone secretion. GLP-1 strongly potentiated glucose-stimulated insulin secretion in the perfused rat pancreas and in vivo in mice (p < 0.001). In contrast, GLP-1 did not enhance arginine-induced insulin release under these experimental conditions. In the perfused rat pancreas, GLP-1 also potentiated glucose-stimulated somatostatin secretion but, again, had no effect on arginine-induced somatostatin release. However, GLP-1 promptly inhibited the arginine-induced glucagon release (p < 0.02). In contrast, CCK enhanced insulin release in response to arginine both in the perfused rat pancreas and in vivo in mice (p < 0.001). In conclusion, GLP-1, in contrast to CCK, failed to enhance arginine-induced insulin release both in vitro and in vivo. This suggests that a signal generated by nutrient metabolism is required for the potentiation of insulin secretion by GLP-1. Furthermore, GLP-1 directly inhibited arginine-induced glucagon release as no concurrent increase in insulin or somatostatin release was noted.