Endocrinology, Vol 134, 2214-2220, Copyright © 1994 by Endocrine Society

ARTICLES

The diurnal rhythm in adrenocorticotropin responses to restraint in adrenalectomized rats is determined by caloric intake

ES Hanson, MJ Bradbury, SF Akana, KS Scribner, AM Strack and MF Dallman
Department of Physiology, University of California, San Francisco 94143- 0444.

There is a diurnal rhythm in ACTH responses to stressors that peaks, in nocturnally feeding rats, at the time of lights on, in the morning (AM). To determine whether this rhythm is subordinate to the rhythm in food intake, we tested the effects of removing food during the night or the day on ACTH responses in the AM or evening (PM) to the stimulus of restraint in 5-day-adrenalectomized rats. An overnight fast reduced the ACTH response to restraint with tail blood sampling in the AM to the low magnitude observed in the PM in rats fed ad libitum; by contrast, a fast of equivalent duration imposed during the day had no effect on the ACTH response to the stressor in the PM. Short term fasts did not alter the normal AM-PM rhythm in basal ACTH levels. The fasts did, however, significantly decrease the pituitary ACTH concentration at both times of day, suggesting that lack of food had stimulated ACTH secretion during the preceding 14 h. Providing calories by either gavage or manipulation of food presentation increased ACTH responses to restraint in fasted adrenalectomized rats in both the AM and PM. Although four of four experiments showed that provision of calories to fasted rats resulted in increased ACTH responses to the stimulus of restraint, none of the manipulations of caloric intake fully restored ACTH responses in fasted rats to the high amplitude observed in ad libitum fed rats in the AM. We conclude that 1) unlike the circadian rhythm in basal activity in the hypothalamic-pituitary-adrenalocortical (HPA) system, the diurnal rhythm in ACTH responsiveness to stimuli is tightly coupled to the endogenous rhythm in energy intake; and 2) caloric deprivation per se appears to activate the HPA system at some time during the 14- to 17-h fast, but does not produce the normal facilitation in the AM response to acute restraint that is induced by chronic or prior stimulation of the HPA axis.

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