INSULIN STIMULATES TESTOSTERONE BIOSYNTHESIS BY HUMAN THECAL CELLS FROM WOMEN WITH POLYCYSTIC-OVARY-SYNDROME BY ACTIVATING ITS OWN RECEPTORAND USING INOSITOLGLYCAN MEDIATORS AS THE SIGNAL-TRANSDUCTION SYSTEM

To determine whether insulin stimulates human ovarian testosterone pro duction in the polycystic ovary syndrome by activating its own recepto r and using inositolglycan mediators as the signal transduction system , thecal cells from polycystic ovary syndrome women were isolated and cultured. Insulin and insulin-like growth factor I stimulated thecal t estosterone biosynthesis. Antibody blockade of the insulin receptor ab olished insulin's stimulatory action, whereas effective antibody block ade of the insulin-like growth factor I receptor did not alter insulin 's stimulation of thecal testosterone biosynthesis. A chiro-inositol c ontaining glycan (INS-S) increased thecal testosterone biosynthesis. P reincubation of cells with an antiinositolglycan antibody (A23939 or a lpha IGP) abolished insulin's stimulatory effect, but not that of hCG. These findings suggest that inositolglycans serve as the signal trans duction system for insulin's stimulation of human thecal testosterone biosynthesis.