Linked Life Data

11872665

Source:http://linkedlifedata.com/resource/pubmed/id/11872665

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-3-1
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
669-75
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11872665-Animals, pubmed-meshheading:11872665-Cells, Cultured, pubmed-meshheading:11872665-Cricetinae, pubmed-meshheading:11872665-Drug Synergism, pubmed-meshheading:11872665-Extracellular Space, pubmed-meshheading:11872665-Fibroblasts, pubmed-meshheading:11872665-Glucagon, pubmed-meshheading:11872665-Glucagon-Like Peptide 1, pubmed-meshheading:11872665-Glucose, pubmed-meshheading:11872665-Insulin, pubmed-meshheading:11872665-Islets of Langerhans, pubmed-meshheading:11872665-Isoproterenol, pubmed-meshheading:11872665-Liver, pubmed-meshheading:11872665-Lung, pubmed-meshheading:11872665-Male, pubmed-meshheading:11872665-Peptide Fragments, pubmed-meshheading:11872665-Protein Precursors, pubmed-meshheading:11872665-Rats, pubmed-meshheading:11872665-Rats, Sprague-Dawley, pubmed-meshheading:11872665-Receptors, Glucagon, pubmed-meshheading:11872665-Signal Transduction
pubmed:year
2002
pubmed:articleTitle
Assessment of the role of interstitial glucagon in the acute glucose secretory responsiveness of in situ pancreatic beta-cells.
pubmed:affiliation
Diabetes Research Center, Vrije Universiteit Brussel, Brussels, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't