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Hypogonadism Induced by a Transplantable, Prolactin-Producing Tumor in Male Rats: Hormonal and Morphological Studies¹

Endocrinology Section, Departments of Medicine and Pediatrics, University of Chicago Chicago, Illinois 60637

Abstract

Pituitary tumors originating from clonal strains of GH₁B₁ and GH₁2C₁ cells differ mainly in the quantities of prolactin production. After these tumors were transplanted to Wistar- Furth inbred rats, only the male rats bearing GH₁B₁tumors which secreted high amount of prolactinand growth hormone exhibited growth retardation and genital atrophy. Female rats bearing the same strain of GH₁B₁ tumor and male rats bearing the predominantly growth hormone-producing GH₁2C₁ tumor were not similarly affected.

As compared to the control and GH₁2C₁ tumorbearing animals, the male rats with GH,B! tumors had strikingly higher levels of circulating prolactin, moderately elevated levels of estrogen and luteinizing hormone but extremely low levels of testosterone. Histological studies of the atrophic testes and accessory sexual glands of the GH₁B₁ tumorbearing rats confirmed the hypoandrogenism foundin these animals. The hormonal data strongly suggest that hyperprolactinemia derived from tumor source was responsible for the primary hypogonadism in male host rats. (Endocrinology 95: 991, 1974)

Footnotes

¹ Aided in part by USPHS Grants HD-07110, HD-06308, HD-70152 and AM-15070.

Received January 28, 1974.

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