Beta adrenergic regulation of rat liver glycogenolysis during aging

Michael S. Katz, Elizabeth M. Dax, Robert I. Gregerman

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

Studies from a number of laboratories demonstrate a biphasic change in β adrenergic regulation of hepatic glycogenolysis over the life span of the male rat. The β 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 β 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 β adrenergic-sensitive adenylate cyclase activation are related to parallel alterations in the density of β adrenergic receptors and also to functional changes in nonreceptor components of the enzyme. The prevailing view that catecholamines stimulate hepatic glycogenolysis by an α adrenergic receptor-mediated, cyclic AMP-independent mechanism is based almost entirely on evidence from young adult male rats. We propose that current concepts of α adrenergic-responsive liver glycogenolysis underestimate a physiological role for β adrenergic responsiveness over the majority of the life span.

Original languageEnglish (US)
Pages (from-to)329-340
Number of pages12
JournalExperimental Gerontology
Volume28
Issue number4-5
DOIs
StatePublished - Jan 1 1993

Keywords

  • G protein
  • adenylate cyclase
  • catecholamines
  • hepatocyte
  • β adrenergic receptor

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology

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