Es. Hanson et al., THE DIURNAL RHYTHM IN ADRENOCORTICOTROPIN RESPONSES TO RESTRAINT IN ADRENALECTOMIZED RATS IS DETERMINED BY CALORIC-INTAKE, Endocrinology, 134(5), 1994, pp. 2214-2220
There is a diurnal rhythm in ACTH responses to stressors that peaks, i
n 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 o
r 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 contra
st, 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 b
oth times of day, suggesting that lack of food had stimulated ACTH sec
retion during the preceding 14 h. Providing calories by either gavage
or manipulation of food presentation increased ACTH responses to restr
aint in fasted adrenalectomized rats in both the AM and PM. Although f
our of four experiments showed that provision of calories to fasted ra
ts resulted in increased ACTH responses to the stimulus of restraint,
none of the manipulations of caloric intake fully restored ACTH respon
ses in fasted rats to the high amplitude observed in ad libitum fed ra
ts 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 coupl
ed to the endogenous rhythm in energy intake; and 2) caloric deprivati
on per se appears to activate the HPA system at some time during the 1
4- to 17-h fast, but does not produce the normal facilitation in the A
M response to acute restraint that is induced by chronic or prior stim
ulation of the HPA axis.