Insulin action in human granulosa cells from normal and polycystic ovaries is mediated by the insulin receptor and not the type-I insulin-like growth factor receptor.
In order to account for the effects of insulin on the polycystic ovary (PCO), despite peripheral insulin resistance in women with polycystic ovary syndrome (PCOS), it has been suggested that insulin may act through the type-I insulin-like growth factor (IGF) receptor and not the insulin receptor. We have tested this hypothesis by investigating the effect of anti-insulin receptor and anti-type-I IGF receptor antibodies on insulin-stimulated steroidogenesis in human granulosa cells in vitro from normal (N) and PCO. Insulin-stimulated estradiol and progesterone production was inhibited by an anti-insulin receptor antibody. In contrast, anti-type-I IGF receptor antibodies had no effect on insulin-stimulated steroidogenesis in granulosa cell cultures from N or PCO. Hence insulin acts via its own receptor in human granulosa cells from both N and PCO.
Department of Obstetrics and Gynaecology, St. Mary's Hospital Medical School, London, UK.
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D000328:Adult; D000911:Antibodies, Monoclonal; D002478:Cells, Cultured; D004958:Estradiol / Q000378:metabolism; D005260:Female; D006107:Granulosa Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D011085:Polycystic Ovary Syndrome / Q000378:metabolism / Q000473:pathology*; D011374:Progesterone / Q000378:metabolism; D011972:Receptor, Insulin / Q000502:physiology*; D012016:Reference Values
D000911:Antibodies, Monoclonal; D007328:Insulin; D011374:Progesterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D011972:Receptor, Insulin