Characterization of Groups of Hyperaiidrogenic Women with Acanthosis Nigricans, Impaired Glucose Tolerance, and/or Hyperinsulinemia*

Abstract

This study examined the prevalence of both basal and glucose-stimulated hyperinsulinemia and acanthosis nigricans (AN) as well as the relationship between insulin and androgen levels in hyperandrogenic women. Sixty-two women who had an elevation of 1 or more plasma androgen levels were studied. The results in these women, grouped for analysis on the basis of obesity and ovulatory status, were compared to those in 36 control women of similar ages and weights. The anovulatory hyperandrogenic women had the clinical and biochemical features of the polycystic ovary syndrome (PCO). Oral glucose tolerance tests were performed with measurement of glucose, insulin, sex hormone-binding globulin (SHBG), and total and non-SHBG-bound sex steroid levels. AN was present in 29% of the hyperandrogenic women, the majority of them obese. Fifty percent of obese PCO women had AN, but they did not otherwise differ from PCO women lacking this dermatological change. Only women with PCO had significant hyperinsulinemia independent of obesity, and obese PCO women with AN had the highest serum insulin levels. Plasma glucose values during the oral glucose tolerance test were significantly increased in obese PCO women independent of the presence of AN, and 20% of these women had frank impairment of glucose tolerance. Ovulatory hyperandrogenic women had normal insulin levels and glucose tolerance. Obese and nonobese women had different relationships between sex steroid and insulin levels; obese women had significant correlations between insulin and non-SHBG testosterone levels (r = 0.30; P less than 0.05), whereas nonobese women had significant correlations between insulin and FSH (r = 0.40; P less than 0.01), dehydroepiandrosterone sulfate (r = 0.33; P less than 0.05), and SHBG (r = 0.37; P less than 0.05) levels, suggesting that the mechanisms underlying the association between sex steroid and insulin levels are complex. These findings suggest that 1) only women with PCO have hyperinsulinemia independent of obesity; hyperinsulinemia is not a feature of hyperandrogenic states in general; 2) AN is a common finding in obese hyperandrogenic women, particularly those with PCO; 3) only obese PCO women are at risk for impairment of glucose tolerance, independent of the presence of AN, suggesting that the negative impact of PCO and obesity on insulin action is additive; and 4) PCO women with AN can be considered as a subgroup of PCO and do not appear to have a distinct endocrine disorder.

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.…”

Female infertility and endocrinological diseases

“…Anovulasyon ve polikistik over olan kadınlarda obezite sıklığı %35-60 olarak bildirilmiştir [20]. Fazla kilolu kadınlarda insülin direncinin eşlik ettiği izlenmiştir [21].…”

C-reactive protein level and obesity as cardiovascular risk factors in polycystic ovary syndrome

“…İnsülin direnci indeksleri obez PKOS' lu hastalarda obez olmayanlara göre anlamlı ölçü-de yüksekti ancak her iki PKOS grubuda kontrol grubuna göre göre daha insulin rezistant idi. Diğer çalışmalarda da, obez PKOS' lular ve normal kilolu PKOS' lular karşılaştırıldığında insülin rezistansı obez grupta daha yüksek bulunmuş ve PKOS prevalansının obezite derecesi ile arttığı gösterilmiş olup obezitenin PKOS gelişiminde artmış bir risk faktörü olduğu belirtilmiştir [18][19][20].…”