POLYCYSTIC OVARIAN DISEASE AND INSULIN RESISTANCE

Abstract

The presence of increased circulating insulin in cases with polycystic ovarian disorder( PCOD) has been well substantiated.1 We lately reported that hyperinsulinemia, beforehand and during an oral glucose tolerance test( OGTT), passed in cases with PCOD in the absence of adiposity and acanthosisnigricans.2 Positive correlations of hyperinsulinemia with serum testosterone( T) and androstenedione(. l4A) levels suggested a unproductive relationship between hyperandrogenism and the inflated insulin responses. These findings appeared to be the consequence of insulin resistance, but no direct measures of insulin perceptivity were performed. substantiation is accumulating that shows that insulin binds to human ovarian tissue3, 4 and, indeed in the face of presumed
supplemental insulin resistance, can stimulate ovarian androgen product.5 thus, we shouldered a study of fifty cases with PCOD unconnected with either adiposity or acanthosis nigricans and six control women to examine( 1) whether hyperinsulinemia is associated with supplemental resistance to insulin and( 2) whether hyperinsulinemia and insulin resistance persist despite long- term
interruption of ovarian androgen production with a long- acting gonadotropin- releasing hormone agonist( GnRH- a).6 continuity of hyperinsulinemia after inhibition of ovarian steroid production would suggest that insulin is involved in the pathogenesis of PCOD, rather than being a result of the primary complaint.