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 | |
| State | Published - 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