ALTERED EXPRESSION OF INSULIN AND INSULIN-LIKE GROWTH FACTOR-I RECEPTORS IN FOLLICULAR AND STROMAL COMPARTMENTS OF POLYCYSTIC OVARIES

In the ovary, insulin and insulin-like growth factor-I (IGF-I) act syn ergistically with FSH to augment estrogen production by granulosa cell s and with LH to augment androgen production by thecal stromal cells. It is also evident that insulin resistance is common in patients with polycystic ovary syndrome (PCO). Thus, in the present study we investi gated the expression of insulin and IGF-I receptors in PCO ovaries and compared them with those in normal ovaries. Ovarian tissues were obta ined from four PCO patients undergoing wedge resection, and from six p atients who underwent radical hysterectomy. Immunohistochemical staini ng for insulin and IGF-I receptors was performed by avidin/biotin immu noperoxidase techniques. In normal ovaries, the expression of insulin and IGF-I receptors in follicular compartment became apparent in the p reantral follicle stage and augmented with the follicular growth, whil e the stromal cells, regardless of the follicle stage, possessed insul in and IGF-I receptors. In PCO ovaries associated with hyperinsulinemi a, no expression of insulin receptors was detected in granulosa or the cal stromal cells, while IGF-I receptor expression increased in thecal stromal cells but decreased in granulosa cells compared to those in n ormal ovaries. However, in PCO ovaries from patients without hyperinsu linemia, insulin receptor expression was apparent in both granulosa an d thecal stromal cells, with a similar intensity to that observed in n ormal ovaries, while IGF-I receptor expression was negligible in granu losa cells but sustained in thecal stromal cells. These findings sugge st that decreased expression of insulin receptors in PCO ovaries assoc iated with hyperinsulinemia may be secondary to receptor down regulati on, whereas defective expression in granulosa cells along with elevate d or persisted expression in thecal stromal cells of IGF-I receptors m ay be common in PCO ovaries and contribute to the endocrine profiles o f PCO in which varying degrees of hyperandrogenism is a predominant fe ature.