GLP-1 (7–36) amide-stimulated insulin secretion in rat islets is sodium-dependent
T Fridolf, B Ahrén - Biochemical and biophysical research communications, 1991 - Elsevier
T Fridolf, B Ahrén
Biochemical and biophysical research communications, 1991•ElsevierWe examined the Na+-dependency of the effects of GLP-1 (7–36) amide in normal,
overnight cultured rat islets. It was found that GLP-1 (7–36) amide stimulated insulin
secretion, 45 Ca 2+-efflux, and 86 Rb+-efflux from prelabelled islets. All these effects were
abolished by omitting Na+ from the medium and replacing it with N-methyl-glucamine. This
suggests that GLP-1 (7–36) amide stimulates insulin secretion by depolarizing the β-cells by
increasing their permeability to Na+.
overnight cultured rat islets. It was found that GLP-1 (7–36) amide stimulated insulin
secretion, 45 Ca 2+-efflux, and 86 Rb+-efflux from prelabelled islets. All these effects were
abolished by omitting Na+ from the medium and replacing it with N-methyl-glucamine. This
suggests that GLP-1 (7–36) amide stimulates insulin secretion by depolarizing the β-cells by
increasing their permeability to Na+.
Abstract
We examined the Na+-dependency of the effects of GLP-1(7–36)amide in normal, overnight cultured rat islets. It was found that GLP-1(7–36)amide stimulated insulin secretion, 45Ca2+-efflux, and 86Rb+-efflux from prelabelled islets. All these effects were abolished by omitting Na+ from the medium and replacing it with N-methyl-glucamine. This suggests that GLP-1(7–36)amide stimulates insulin secretion by depolarizing the β-cells by increasing their permeability to Na+.
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