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Journal of Andrology, Vol 3, Issue 1 79-83, Copyright © 1982 by The American Society of Andrology

Abnormalities of the Hypothalamic—Pituitary—Leydig Cell Axis in Young Adult Rats with Vitamin A Deficiency

CARLOS E. MENENDEZ 1, GREGORY DUCKETT 1, AND ALLEN W. ROOT 1

1 Department of Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas and the Departments of Comprehensive Medicine, Medicine, and Pediatrics, University of South Florida College of Medicine, Tampa, Florida

The hypothalamic concentration of gonadotrophin releasing hormone (GnRH), the in vivo pituitary responses to GnRH, and the in vivo Leydig cell responses to bovine luteinizing hormone (LH) and to endogenous LH were determined in young adult male rats who had been on a vitamin-A-deficient (VAD) diet for 64 days and in age-matched controls. Hypothalamic GnRH content was 3.06 ± 0.25 ng/ hypothalamus in VAD (mean ± SEM) and 3.26 ± 0.25 ng/hypothalamus in controls. Baseline serum LH concentrations were 24.6 ± 4.7 ng/ml in VAD and 11.3 ± 2.3 ng/ml in controls (P < 0.02). Baseline serum follicle stimulating hormone (FSH) levels were 373 ± 61 ng/ml in VAD and 329 ± 16 ng/ml in controls. Fifteen minutes after administration of GnRH serum LH was 215 ± 16.3 ng/ml in VAD vs. 148 ± 18.3 ng/ml in controls (P < 0.02). Serum FSH levels 15 minutes after administration of GnRH were 866 ± 67 ng/ml in VAD vs. 566 ± 58 ng/ml in controls (P < 0.01). Baseline serum testosterone (T) concentrations were 1.0 ± 0.2 ng/ml vs. 1.7 ± 0.3 ng/ml in controls (n.s.). Sixty minutes after exogenous LH administration, serum T concentrations were 21.7 ± 1.0 ng/ml in VAD vs. 17.8 ± 1.0 ng/ml in controls (P < 0.05). Sixty minutes after administration of GnRH, which elevated endogenous LH serum concentrations, serum T concentrations were similar in both groups (7.8 ± 0.9 ng/ml for VAD vs. 9.7 ± 0.5 ng/ml for controls). The elevated serum LH concentrations, together with the increased pituitary responses to GnRH, are compatible with an appropriate hypothalamic-pituitary response to a direct impairment in testicular function secondary to the VAD. However, the increased in vivo Leydig cell responses to exogenous LH stimulation in these young adult males with VAD remains unexplained.

     Key words: vitamin A deficiency (VAD), hypogonadism, testosterone, Leydig cell, hypothalamus, pituitary, gonadotrophin

Submitted on April 15, 1980
Revised on March 26, 1981
Accepted on May 1, 1981






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Copyright © 1982 by The American Society of Andrology.