Vnitr Lek 1995, 41(2):126-128

[Hyperandrogenic states in women (polycystic ovary syndrome) and insulin resistance].

A Kreze, J Hrnciar, M Dobáková: Interná klinika A, Nemocnica F.D. Roosevelta, Banská Bystrica.

Klíčová slova: Female; Humans; Hyperandrogenism, physiopathology, ; Insulin Resistance; Insulin-Like Growth Factor I, physiology, ; Polycystic Ovary Syndrome, physiopathology,

In the submitted paper the authors try to explain the relationship between hyperinsulinism as the cause and the polycystic ovary syndrome as the consequence of hyperinsulinism. This takes place via the insulin like growth factor I, the luteinizing hormone, sex binding hormone globulin, insulin like growth factor I binding protein and growth hormone. By varying interactions of the regulatory hormones gradually the granulosa cells are destroyed and replaced by androstendione producing thecal and stromal cells with impaired folliculogenesis. Chronic hyperestrogenism interferes also with hypothalamic regulation in the nucleus arcuatus. As almost identical changes are found in polycystic ovary syndrome and puberty, genetic and/or environmental factors certainly play a part. Their more detailed specification is a task for the future.