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The Impact of Insulin Secretion on the Ovarian Response to Exogenous Gonadotropins in Polycystic Ovary Syndrome

Department of Obstetrics and Gynaecology (A.M.F., P.V., V.P., M.G., R.A., A.C., S.M.) and Department of Pediatrics (A.R.), Catholic University, 00168 Rome, Italy; and Institute for Research (A.L.), 96018 Troina, Italy

Address all correspondence and requests for reprints to: A. M. Fulghesu, Clinica Ostetrica Ginecologica, Università Cattolica del Sacro Cuore, Lgo Gemelli 8, 00168 Roma, Italy.

The aim of the study was to evaluate the influence of insulin level on the ovarian response to FSH when inducing ovulation in patients affected by polycystic ovarian syndrome (PCOS). To evaluate the presence of hyperinsulinemia, 34 patients affected by PCOS were studied by an oral glucose tolerance test, then patients were stimulated for 52 cycles using FSH to induce ovulation. The ovarian response to therapy was evaluated by ultrasounds and as estradiol (E₂) and androstenedione (A) plasma level determinations. On the basis of the insulinemic response to the glucose challenge, 20 patients were considered to be hyperinsulinemic and 14 normoinsulinemic. The hormonal features of each group were similar. The ovulation rate was similar in hyperinsulinemic and normoinsulinemic subjects, whereas the incidence of ovarian hyperstimulation was significantly higher in the hyperinsulinemic group. The increase in ovarian dimensions observed in hyperinsulinemic subjects after gonadotropin stimulation was more marked than that observed in normoinsulinemic ones. This was caused by the development of a larger number of immature follicles. E₂ levels gradually increased after gonadotropin stimulation in both groups of subjects; however, higher levels were observed in hyperinsulinemic patients. During stimulation, the higher E₂/A ratio suggests the presence of a greater aromatization activity in hyperinsulinemic patients. In conclusion, the present study suggests that, in PCOS, the insulinemic pattern may influence the ovarian response to gonadotropin administration; thus, hyperinsulinemic subjects may be at greater risk of ovarian hyperstimulation syndrome than normoinsulinemic subjects.

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