Endocrine Changes Associated with Germ Cell Loss during Vitamin A-Induced Recovery of Spermatogenesis*
- 1 April 1983
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 112 (4) , 1163-1171
- https://doi.org/10.1210/endo-112-4-1163
Abstract
Vitamin A deficiency (VAD) causes progressive male germ cell depletion which is rapidly reversed by vitamin A replacement. The time course of the associated endocrine changes in the hypothalamic-pituitary-testicular axis was studied. Retro-orbital sinus blood samples were obtained at 10-day intervals from rats on a vitamin A-deficient (VAD) diet from 50–140 days of age and for 60 days at 2-day intervals from deficient rats given vitamin A replacement at age 130 days. Serum testosterone levels in rats fed a vitamin A-deficient diet from 20–140 days of age were within the normal range, although consistently lower than those of age-matched controls. Serum FSH and LH levels in VAD rats were comparable to those of controls until 60 days of age; thereafter, FSH levels increased and by 90 days of age were significantly higher than those of controls. At 65 days of age, complete spermatogenesis was present in VAD animals. By 110 days of age, most tubules contained only Sertoli cells, spermatogonia, and, in some tubules, preleptotene spermatocytes. At 130 days of age, spermatogenesis was reinitiated by vitamin A replacement and progressed normally to completion by 40 days thereafter. During this regrowth of germinal epithelium, serum LH and testosterone levels did not change significantly and were normal. In contrast, FSH levels, which had become elevated during VAD, increased further during the first 10 days post-vitamin A replacement, remained elevated for at least 30 days, and gradually returned to normal. The complex series of changes in FSH secretion cannot be attributed to changes either in vitamin A status or in serum testosterone levels, nor can they be correlated with the status of the germinal epithelium. Since FSH hypersecretion persisted in the presence of qualitatively normal spermatogenesis, these data suggest that the germ cell-Sertoli cell component of FSH regulation (inhibin?) is independent of that Sertoli cell function which regulates sperm production.Keywords
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