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Endocrinology, Vol 110, 1542-1546, Copyright © 1982 by Endocrine Society

ARTICLES

Pituitary-testicular function in protein-deficient rats. Follicle- stimulating hormone hyperresponse to castration and supersensitivity of gonadotropin secretion to androgen negative feedback

AR Glass, A Steinberger, R Swerdloff and RA Vigersky

Previous studies have shown that weanling male rats fed a low protein diet ad libitum develop hypogonadotropic hypogonadism. Two unusual features of this state were 1) subnormal serum FSH in noncastrate rats but not in castrate rats, suggesting that FSH was being suppressed by a testicular factor, and 2) serum FSH increases after castration that were greater in protein-deficient rats than in controls. In the current study, protein-deficient rats showed FSH hyperresponse to castration, compared to either ad libitum or pair-fed controls, after periods of low protein feeding from 1-8 weeks and periods of castration from 1-8 weeks. FSH hyperresponse to castration was rapidly induced after the start of low protein feeding and was present whether castration was performed before or after low protein feeding was begun. In none of these circumstances did protein-deficient rats show LH hyperresponse to castration. Inhibin production of Sertoli cell cultures prepared from protein-deficient rats was less (P less than 0.02) than in ad libitum or pair-fed controls, suggesting that inhibin overproduction was not the cause of subnormal serum FSH in noncastrate protein-deficient rats. However, castrated rats fed a low protein diet were more sensitive to the negative feedback effects of testosterone on gonadotropin secretion than were ad libitum or pair-fed controls. We conclude that low serum gonadotropins in protein-deficient male rats may be related to hypersensitivity of these animals to the negative feedback effects of testosterone on gonadotropin secretion. In addition, FSH hyperresponse to castration, without corresponding LH hyperresponse, seems to be typical of protein deficiency, suggesting that protein deficiency may be a useful model for exploring the differential control of gonadotropin secretion.




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Copyright © 1982 by The Endocrine Society