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Am J Physiol Endocrinol Metab 281: E516-E523, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 3, E516-E523, September 2001

Attenuation of age-related declines in glucagon-mediated signal transduction in rat liver by exercise training

Deborah A. Podolin1,2, Brandon K. Wills1, Ian O. Wood1, Mark Lopez3, Robert S. Mazzeo1, and David A. Roth1,3

1 University of Colorado, Boulder, Colorado 80303; 2 University of New England, Biddeford, Maine 04005; and 3 Collateral Therapeutics, San Diego, California 92121

This study investigated alterations in glucagon receptor-mediated signal transduction in rat livers from 7- to 25-mo-old animals and examined the effects of exercise training on ameliorating these changes. Sixty-six young (4 mo), middle-aged (12 mo), and old (22 mo) male Fischer 344 rats were divided into sedentary and trained (treadmill running) groups. Isolated hepatic membranes were combined with [125I-Tyr10]monoiodoglucagon and nine concentrations of glucagon to determine maximal binding capacity (Bmax) and dissociation constant (Kd). No alterations were found in Bmax among groups; however, middle-aged trained animals had significantly higher glucagon affinity (lower Kd; 21.1 ± 1.8 nM) than did their untrained counterparts (50.2 ± 7.1 nM). Second messenger studies were performed by measuring adenylyl cyclase (AC) specific activity under basal conditions and with four pharmacological stimulations to assess changes in receptor-dependent, G protein-dependent, and AC catalyst-dependent cAMP production. Age-related declines were observed in the old animals under all five conditions. Training resulted in increased cAMP production in the old animals when AC was directly stimulated by forskolin. Stimulatory G protein (Gs) content was reduced with age in the sedentary group; however, training offset this decline. We conclude that age-related declines in glucagon signaling capacity and responsiveness may be attributed, in part, to declines in intrinsic AC activity and changes in G protein [inhibitory G protein (Gi)/Gs] ratios. These age-related changes occur in the absence of alterations in glucagon receptor content and appear to involve both G protein- and AC-related changes. Endurance training was able to significantly offset these declines through restoration of the Gi/Gs ratio and AC activity.

adenylyl cyclase; hepatic membranes; GTP-binding proteins; gluconeogenesis; aging; glucose homeostasis


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