Linked Life Data

8224032

Source:http://linkedlifedata.com/resource/pubmed/id/8224032

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4-5
pubmed:dateCreated
1993-12-22
pubmed:abstractText
Studies from a number of laboratories demonstrate a biphasic change in beta adrenergic regulation of hepatic glycogenolysis over the life span of the male rat. The beta adrenergic response is prominent in immature animals, declines rapidly during subsequent development to a minimum by the time of young adulthood, and then reemerges during postmaturational development. Age changes in beta adrenergic-responsive adenylate cyclase activity follow a "U"-shaped curve similar to that described by changes in liver glycogenolytic responsiveness during aging. Developmental and postmaturational changes in beta adrenergic-sensitive adenylate cyclase activation are related to parallel alterations in the density of beta adrenergic receptors and also to functional changes in nonreceptor components of the enzyme. The prevailing view that catecholamines stimulate hepatic glycogenolysis by an alpha adrenergic receptor-mediated, cyclic AMP-independent mechanism is based almost entirely on evidence from young adult male rats. We propose that current concepts of alpha adrenergic-responsive liver glycogenolysis underestimate a physiological role for beta adrenergic responsiveness over the majority of the life span.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0531-5565
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
329-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Beta adrenergic regulation of rat liver glycogenolysis during aging.
pubmed:affiliation
Department of Medicine, University of Texas Health Science Center at San Antonio.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review