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Manuscript received 14 November 1997. Initial reviews completed 17 January 1998. Revision accepted 6 May 1998.
Department of Physiology, The University of Texas Health Science Center, San Antonio, TX 78284-7756
Chronic food restriction (FR) of rats and mice results in moderate hyperadrenocorticism, which may play a role in activating cellular mechanisms that retard aging. Previously, we reported that the FR-induced hyperadrenocorticism is not due to an activated hypothalamo-pituitary unit. Therefore, we investigated in a series of experiments whether adrenal responsiveness to adrenocorticotropic hormone (ACTH), in vitro and in vivo, is enhanced by FR. Three mo-old male Fischer 344 rats were either given free access to food (AL rats) or restricted to 60% of food consumed by AL rats (FR rats) from 6 wk of age. They were killed by decapitation in the morning (AM) and afternoon (PM) when endogenously circulating corticosterone levels are at their nadir and peak, respectively. In vitro, adrenal glands from FR rats (1.5 mo FR) produced more corticosterone per mg at all doses of ACTH than those from AL rats in both the AM and PM (diet main effect, P < 0.001). FR (1.5 to 2.5 mo) also enhanced adrenal responsiveness to physiologic (diet main effect, P < 0.05) and superphysiologic (diet main effect, P < 0.001) levels of ACTH administered in vivo to dexamethasone-treated rats. ACTH-receptor (ACTH-R) mRNA, normalized to adrenal mass or to total RNA, was not influenced by FR (1.5 mo). However, adrenal ACTH-R mRNA, as well as adrenal mass, per unit body weight was greater in FR than in AL rats (diet main effect, P < 0.001). These results indicate that enhanced adrenocortical responsiveness to ACTH plays a major role in the hyperadrenocortical state of chronically FR rats.
Key words: male Fischer 344 rats, food restriction, adrenal sensitivity, corticosterone.
The Journal of Nutrition Vol. 128 No. 9 September 1998,
pp. 1415-1420
Copyright ©1998 by the American Society for Nutritional Sciences
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