Insulin Resistance in Nonobese Patients with Polycystic Ovarian Disease*

Abstract

To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Mean serum testosterone (T), androstenedione (A), dehydroepiandrosterone (D), D sulfate, and LH levels were significantly elevated in the PCO patients compared to those in control subjects. In PCO patients, the mean +/- SE basal insulin level (18.7 +/- 2.9 microU/ml) and the sum of the insulin levels in response to glucose (674 +/- 119 microU/ml) were significantly greater than those in the control group (11.0 +/- 0.8 microU/ml and 248 +/- 29 microU/ml, respectively). In all subjects, serum levels of T and A, but not D and D sulfate, were significantly correlated to basal insulin levels and insulin sums. Serum cortisol, GH, and PRL levels were similar in both groups. These results indicate that in PCO, a significant degree of insulin resistance exists, which clearly is not related to obesity. The positive correlation of serum T and A levels to circulating insulin levels in this study suggests that the insulin resistance in PCO may be, in part, a consequence of hyperandrogenism.

Body Shape and Size and Insulin Resistance as Early Clinical Predictors of Hyperandrogenic Anovulation in Ethnic Minority Adolescent Girls

“…(24)(25)(26)(27) Obesity begets insulin resistance, the associated hyperinsulinemia suppresses hepatic production of SHBG, and in turn free plasma testosterone becomes elevated. (28)(29)(30) Women with PCOS have insulin resistance that is more severe than can be accounted for by obesity alone (25,31,32) and this leads to even greater reductions in SHBG and higher androgens. In turn insulin may drive androgen secretion in PCOS, thus causing a feed-forward mechanism promoting hyperandrogenemia.…”

Metformin therapy for the reproductive and metabolic consequences of polycystic ovary syndrome

“…Over the ensuing decades, it became clear that this 'reproductive' syndrome was often accompanied by metabolic features that are a consequence of insulin resistance and hyperinsulinaemia [2][3][4], for example, impairment in oral glucose tolerance, type 2 diabetes [5,6], the metabolic syndrome [7,8] and dyslipidaemia [9,10]. The magnitude of insulin resistance in PCOS is greater than that caused by excess adiposity alone; it is characterised by reduced sensitivity and responsiveness to insulin-mediated glucose utilisation, primarily in the skeletal muscle, adipose tissue and in the liver [11].…”

Predictors of Insulin Resistance and Metabolic Complications in Polycystic Ovarian Syndrome in an Eastern Indian Population

“…As much as 64 % of PCOS patients were found to have insulin resistance that could not be predicted by weight alone [9]. Similarly, strong associations of insulin with various circulating androgens and waist hip ratio (WHR) in PCOS have been reported that were found to be independent of body mass index (BMI) [10][11][12][13].…”