Linked Life Data

6126124

Source:http://linkedlifedata.com/resource/pubmed/id/6126124

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1982-10-29
pubmed:abstractText
Glucose production decreases markedly following acute reduction in insulin and glucagon secretion (induced by somatostatin). After about an hour, however, glucose production is restored nearly to basal rates. To study the mechanism by which this occurs, islet hormone deficiency was superimposed on beta-adrenergic blockade. It was found that the hypoglycemia that accompanies insulin and glucagon deficiency is an adequate stimulus for catecholamine secretion. During combined hormone deficiency and beta-blockade, glucose production fell and remained very low for 2-3 h. This resulted in a profound hypoglycemia (glucose less than 30 mg/dl). We conclude from these studies that restoration of glucose production during sustained insulin and glucagon deficiency is not attributable to a) onset of insulin deficiency because insulin is equally depressed in both experimental settings, b) glucose autoregulation even though adequate substrate is available, or c) an alpha-adrenergic mechanism because plasma catecholamines were very high and alpha-receptors were not blocked. Rather, the glucose counterregulation during insulin and glucagon deficiency must be heavily dependent on a beta-adrenergic mechanism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
243
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E225-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Glucoregulation during insulin and glucagon deficiency: role of catecholamines.
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