EVIDENCE OF A DISTINCT DERANGEMENT OF OPIOID TONE IN HYPERINSULINEMICPATIENTS WITH POLYCYSTIC OVARIAN SYNDROME - RELATIONSHIP WITH INSULINAND LUTEINIZING-HORMONE SECRETION

Recent data indicate that an altered opioid tone could be involved in the LH hypersecretion and metabolic alterations seen in polycystic ova ry syndrome (PCOS). The aim of the present study was to investigate th e presence of a common mechanism of action of opioids on altered insul in and gonadotropin release in patients suffering from PCOS. Twenty-ei ght women affected by PCOS and 8 normal ovulatory women were studied; an oral glucose tolerance test (OGTT) and GnRH tests were performed du ring the follicular phase before and after 6 weeks of naltrexone treat ment (50 mg/day, orally). Plasma levels of sex hormone-binding globuli n and steroids were assayed in the basal samples, whereas FSH and LH w ere analyzed during the GnRH stimulus. Insulin and glucose were assaye d by the OGTT. Based on the insulinemic response to OGTT, 17 women wer e classified as hyperinsulinemic and 11 as normoinsulinemic. No differ ence in glucose and hormone plasma concentrations was observed before and after naltrexone treatment in both groups. Only basal sex hormone- binding globulin values were higher in normoinsulinemic compared to hy perinsulinemic subjects. Administration of the opioid antagonist signi ficantly reduced the insulin response to OGTT only in the hyperinsulin emic group. No difference were found in the LH increment after the GnR H stimulus in both group of patients before treatment; on the contrary , naltrexone administration reduced the LH response to GnRH in hyperin sulinemic women but failed to be effective in normoinsulinemic subject s. Only 5 patients showed no concordance of drug-induced changes in in sulin and LH secretion. In control subjects, naltrexone failed to have any effect on insulin or LH secretion. These data support the involve ment of endogenous opioids in the regulation of insulin and LH secreti on in a specific group of PCOS patients exhibiting an exaggerated insu lin response to OGTT.