Journal
ENDOCRINOLOGY
Volume 142, Issue 11, Pages 4652-4662Publisher
ENDOCRINE SOC
DOI: 10.1210/en.142.11.4652
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Funding
- NCRR NIH HHS [K01 RR000163, P51 RR000163, RR-00163] Funding Source: Medline
- NIAMS NIH HHS [R01 AR051943] Funding Source: Medline
- NICHD NIH HHS [HD-38127] Funding Source: Medline
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Mice lacking steroid 5 alpha -reductase 1 and 2 were produced by gene targeting and breeding. Male mice without 5 alpha -reductase 2 or without both enzymes had fully formed internal and external genitalia and were fertile, but had smaller prostates and seminal vesicles than controls. T accumulated to high levels in the reproductive tissues of the mutant mice. DHT administration increased seminal vesicle and coagulating gland weights in mice deficient in 5 alpha -reductase 2 and increased the weights of the prostate, seminal vesicle, and coagulating gland in animals deficient in both enzymes. An inhibitor of both 5 alpha -reductases (GI 208335X) decreased prostate and coagulating gland weights of control mice, but had no effect in those lacking 5 alpha -reductase 1 and 2. Castration reduced the sizes of these tissues in animals of all genotypes. Androgen-dependent gene expression was decreased in the seminal vesicles of mice lacking one or more 5 alpha -reductases and was restored by administration of T or DHT. Female mice missing both enzymes exhibited parturition and fecundity defects similar to those of animals without 5 alpha -reductase 1. We conclude that T is the only androgen required for differentiation of the male urogenital tract in mice and that the synthesis of DHT serves largely as a signal amplification mechanism.
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