Pituitary-adrenal function and hypothalamic beta-endorphin release in vitro following food deprivation

Pituitary-adrenal function and hypothalamic beta-endorphin release in vitro following food deprivation

Mitev Y; Almeida OF; Patchev V

Brain Research Bulletin

1993

Male; Time Factors; Animals; Rats; Non-U.S. Gov't; Research Support; Body Weight; Blood Glucose/metabolism; Corticosterone/blood; In Vitro; Pituitary-Adrenal System/physiology; Adrenal Glands/physiology; beta-Endorphin/secretion; Corticotropin-Releasing Hormone/pharmacology; Dexamethasone/pharmacology; Food Deprivation; Hypothalamus/drug effects/secretion; Organ Size; Thymus Gland/physiology; Wistar

Basal and dexamethasone-suppressed adrenal glucocorticoid secretion and hypothalamic beta-endorphin (BE) release in vitro were investigated in rats deprived of food for 24, 48, 72, and 96 h. Fasting for up to 48 h neither caused significant changes in serum corticosterone levels nor in the suppressive effect of dexamethasone. Food deprivation for 72-96 h resulted in increased basal serum corticosterone, diminished suppression by dexamethasone, and a significant involution of the thymus. Basal in vitro BE release from hypothalamic explants was significantly increased after the first day of food deprivation, and in vitro perifusion with corticotropin-releasing hormone (CRH) failed to enhance BE release further. With continuing food deprivation, basal BE release remained significantly greater than that from hypothalami originating from normally fed control rats. The stimulatory effect of CRH on BE release was only partially restored after 2 days of fasting. The results suggest that food deprivation for more than 2 days increases basal glucocorticoid secretion, and signs of impairment in hypothalamic-pituitary-adrenal regulation become apparent. These findings might be implicated in the pathogenetic mechanisms of endocrine dysregulation in diseases related to caloric reduction.

1993

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