Linked Life Data

6392344

Source:http://linkedlifedata.com/resource/pubmed/id/6392344

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1985-1-31
pubmed:abstractText
To determine if glucagon secretion is under physiological control of intra-islet insulin, pancreata from normal rats were perfused at a 100 mg/dl glucose concentration with either guinea pig antiinsulin serum or normal guinea pig serum in a nonrecirculating system. Perfusion of antiserum was followed within 3 min by a significant rise in glucagon that reached peak levels three times the base-line values and assumed a hectic pattern that returned rapidly to base-line levels upon termination of the antiserum perfusion. Nonimmune guinea pig serum had no effect. To gain insight into the probable site of insulin neutralization, 125I-labeled human gamma-globulin was added to antiserum or nonimmune serum and perfused for 3 min. More than 83% of the radioactivity was recovered in the effluent within 3 min after termination of the infusion, and only 0.05 +/- 0.015% of the radioactivity injected was present in the pancreas 10 min after the perfusion. The maximal amount of insulin that could be completely bound to insulin antibody at a dilution and under conditions simulating those of the perfusion experiments was 20 mU/min. It is concluded that insulin maintains an ongoing restraint upon alpha cell secretion and in its absence causes hectic hypersecretion of glucagon. This restraint probably occurs largely in the intravascular compartment. Loss of this release-inhibiting action of insulin may account for initiation of hyperglucagonemia in insulin-deficient states.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-1097860, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-1184740, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-13846364, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-200493, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-320077, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-4270691, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-4935445, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-4986215, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-5320561, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-6109226, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-6126931, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-6368593, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-6759221, http://linkedlifedata.com/resource/pubmed/commentcorrection/6392344-7019246
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2296-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Insulin within islets is a physiologic glucagon release inhibitor.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't