作者: Ke-nan Qin , Robert L Rosenfield
DOI: 10.1016/S0303-7207(98)00177-4
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摘要: The hyperandrogenism of polycystic ovary syndrome (PCOS) appears to be due dysregulation steroidogenesis within the ovaries and adrenal glands. P450c17 is key enzyme that regulates androgen synthesis. It only known have capacity convert C21-precursors pre-hormones, 17-ketosteroids. a single with two activities, 17-hydroxylase 17,20-lyase. Thus, its regulation significant factor in expression hyperandrogenism. Androgen secretion LH-dependent ACTH-dependent androgenic response each these tropic hormones seems modulated by intra-ovarian or intra-adrenal autocrine paracrine mechanisms. This modulation serves regulate steroid hormone tissue-specific ways. Insulin, IGFs inhibin are among many growth factors capable augmenting LH ACTH. insulin/IGF system stimulates mRNA activities An integrating link between insulin resistance hyperandrogenemia may serine phosphorylation, which inhibits activity receptor promotes 17,20-lyase P450c17. However, it must kept mind there some evidence for existence P450c17-independent pathways biosynthesis.