Beta adrenergic regulation of rat liver glycogenolysis during aging

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

doi:10.1016/0531-5565(93)90060-Q

Beta adrenergic regulation of rat liver glycogenolysis during aging

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

Medicine

Research output: Contribution to journal › Article › peer-review

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 language	English (US)
Pages (from-to)	329-340
Number of pages	12
Journal	Experimental Gerontology
Volume	28
Issue number	4-5
DOIs	https://doi.org/10.1016/0531-5565(93)90060-Q
State	Published - 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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title = "Beta adrenergic regulation of rat liver glycogenolysis during aging",

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.",

keywords = "G protein, adenylate cyclase, catecholamines, hepatocyte, β adrenergic receptor",

author = "Katz, {Michael S.} and Dax, {Elizabeth M.} and Gregerman, {Robert I.}",

note = "Funding Information: Acknowledgments--We are grateful to Dr. Reubin Andres, whose enlightened leadership of the Clinical Physiology Branch, National Institute on Aging has provided a generation of gerontological investigators with a research environment supportive of creative thought and good humor. We also thank John Partilla, Marco Pifieyro, Dien van Pham, Shirley Jean Schmidt, Sarah Kohn, Tazuko Hymer, and Christopher McNair for their important contributions to our studies, and David Katz for capping thousands of scintillation vials without compensation or prior acknowledgment. This manuscript is dedicated to the memory of our colleague Dr. Maurice Attic. This work was supported in part by Medical Research funds from the Department of Veterans Affairs. Copyright: Copyright 2014 Elsevier B.V., All rights reserved.",

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PY - 1993

Y1 - 1993

N2 - 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.

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KW - β adrenergic receptor

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Beta adrenergic regulation of rat liver glycogenolysis during aging

Abstract

Keywords

ASJC Scopus subject areas

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