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A patient with familial male pseudohermaphroditism was considered to be a normal female up to the time of puberty. At puberty, she had normal breast development but there was simultaneous enlargement of the clitoris and the body hair developed with a male distribution. The internal genitalia were male in type. Under basal conditions, the plasma concentration of testosterone (T) was low for a male subject but plasma levels of dehydroepiandrosterone (DHA) and dehydroepiandrosterone sulfate (DHAS) were 2-3 times higher than those of normal men. The plasma level of androstenedione (A) was 10 times normal. Following gonadectomy, the pattern of plasma androgens was similar to that of a normal woman. Prior to operation, the basal urinary excretion of estrone, estradiol and estriol was much increased above that of a normal man but it became normal after gonadectomy. Eighteen months after gonadectomy, both before and after adrenal stimulation, the plasma androgens showed the pattern and concentrations expected in the normal adult female. The same could be said of the peripheral in terconversion between T & A. The data strongly suggest that the patient had an incomplete 17-ketosteroid reductase defect and that this defect was limited to the testes. (J Clin Endocr 32: 604, 1971)

The effects of insulin, somatomedin-C (Sm-C), epidermal growth factor (EGF), fibroblast growth factor (FGF), vitamin E, and retinoic acid on growth and function of immature cultured pig Sertoli cells were investigated. All these factors, except vitamin E, stimulated Sertoli cell DNA synthesis and proliferation. The mitogenic effects of insulin observed only at micromolar concentrations were similar to those induced by nanomolar concentrations of Sm-C or EGF, but significantly less than those induced by FGF. The effects of EGF and Sm-C were almost additive, whereas those of Sm-C and FGF were synergistic. After a 6-day treatment, FGF and retinoic acid induced a significant increase in the number of follicle-stimulating hormone (FSH) receptors per cell, and in FSH-induced cyclic adenosine 3',5'-monophosphate (cAMP) production. Sm-C, which alone had no effect on these two parameters, potentiated FGF action. Basal plasminogen activator activity was enhanced after the 6-day treatment with EGF plus insulin and, particularly, with FGF plus insulin. Similarly, the response of the latter group to FSH was significantly higher than in any other group of cells. FGF was also able to stimulate cell multiplication and enhanced the FSH receptor number of Sertoli cells isolated from 15- and 26-day-old rats. Thus, FGF is the most potent known mitogenic factor for cultured Sertoli cells, and it stimulates the phenotypic expression of these cells.