Abstract
THE aetiology of the polycystic ovary syndrome of Stein-Leventhal1 is still unknown. Histologically, the ovaries from Stein-Leventhal patients are comparable in many respects to polycystic rat ovaries which have been observed in sexually mature rats following the administration of testosterone propionate during the neonatal period or continuous exposure of adult rats to a constant light environment2. Furthermore, increased in vitro conversion of progesterone to androgen and oestrogen has been described in incubations of both human and rat polycystic ovaries3. A clear insight into altered ovarian physiology which may precede the development of polycystic ovaries in the rat might therefore provide a better understanding of the human syndrome.
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