Dehydroepiandrosterone-Sulphate-Secretion and State of Adrenal Function in the Rat
II. The Influence of Dietary Restriction
1987 年 2 巻 2 号 p. 153-161
詳細
1987 年 2 巻 2 号 p. 153-161
After more than one month under growth-restraining feeding conditions the influence of undernutrition (50% feed restriction) on dehydroepiandrosterone sulphate (DHEA-S) and 11-OHCS (corticosterone) secretion was investigated in male Wistar rats. Diet-restricted (DR) rats, untreated before the taking of blood samples, showed clearly elevated 11-OHCS plasma levels in the morning (lights-on) compared to ad libitum-fed (AL) control rats, whereas the evening (lights-off) 11-OHCS levels were almost identical in both groups. The corresponding DHEA-S blood concentrations were equal under both feeding schedules in the morning as well as in the evening. However DHEA-S response to adrenocorticotropic hormone (ACTH) administration was significantly elevated in DR rats compared with AL rats. No such difference was detectable for ACTH-stimulated 11-OHCS blood levels. Measurement of total adrenal cholesterol content revealed a markedly higher concentration of this hormone precursor in the glands of untreated DR rats than in the adrenals of the AL control group, thus clearly indicating the existence of a chronically elevated endogenous ACTH secretion under dietary restriction, since continued in vivo ACTH stimulation is known to increase the cholesterol content of the adrenal cortex. Furthermore the occurrence of a nutritional stress is obviously reflected by the elevated 11-OHCS levels in the circulation of DR rats at “lights-on.” The observations in DR rats coupled with the findings in ACTH-pretreated rats under metyrapone treatment (J. Clin. Biochem. Nutr., 2, 141-152, 1987) strongly support our already proposed concept that stress or stimulation of the cortico adrenal activity provokes an increase in the capacity for secretion of DHEA-S measurable after an appropriate stimulation. Contrary to a recently published hypothesis undernutrition appears to be not necessarily associated with a suppression of enzymes involved in DHEA-S formation.
