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Title: Assessment of the role of interstitial glucagon in the acute glucose secretory responsiveness of in situ pancreatic beta-cells
Authors: Moens, Karen
Berger, Veerle
Ahn, Jung-Mo
Van Schravendijk, Chris
Hruby, Victor J
Pipeleers, Daniel
Schuit, Frans # ×
Issue Date: Mar-2002
Publisher: American Diabetes Association
Series Title: Diabetes vol:51 issue:3 pages:669-675
Abstract: Glucagon is a potent stimulator of insulin release in the presence of a permissive glucose concentration, activating beta-cells in vitro via both glucagon- and glucagon-like peptide-1 (GLP-1)-receptors. It is still unclear whether locally released glucagon amplifies the secretory responsiveness of neighboring beta-cells in the intact pancreas. The present study investigates this question in the perfused pancreas by examining the effects of antagonists for glucagon receptors ([des-His(1),des-Phe(6),Glu(9)]glucagon-NH(2), 10 micromol/l) and GLP-1-receptors [exendin-(9-39)-NH(2), 1 micromol/l] on the insulin secretory response to glucose. The specificity of both antagonists was demonstrated by their selective interaction with glucagon-receptor signaling in rat hepatocytes and GLP-1-receptor signaling in Chinese hamster lung (CHL) fibroblasts. In purified rat beta-cells, the glucagon-receptor antagonist (10 micromol/l) inhibited the effect of 1 nmol/l glucagon upon glucose-induced insulin release by 78 plus minus 6%. In the perfused rat pancreas, neither of these antagonists inhibited the potent secretory response to 20 mmol/l glucose, although they effectively suppressed the potentiating effect of, respectively, an infusion of glucagon (1 nmol/l) or GLP-1 (1 nmol/l) on insulin release. When endogenous glucagon release was enhanced by isoproterenol (100 nmol/l), no amplification was seen in the simultaneous or subsequent insulin secretory response to glucose. It is concluded that, at least under the present selected conditions, the glucose-induced insulin release by the perfused rat pancreas seems to occur independent of an amplifying glucagon signal from neighboring alpha-cells.
URI: 
ISSN: 0012-1797
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Gene Expression Unit
× corresponding author
# (joint) last author

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