Glucose Intolerance In Polycystic Ovary Syndrome Research Articles

Association of Androgen Excess with Glucose Intolerance in Women with Polycystic Ovary Syndrome

Women with polycystic ovary syndrome (PCOS) show high prevalence of glucose intolerance. This study aimed to investigate the association of androgen excess with glucose intolerance in PCOS. A total of 378 women with PCOS participated in the study. Free androgen index (FAI) was selected as indicator of hyperandrogenism. Insulin sensitivity was assessed by 1/homeostasis model assessment of insulin resistance (1/HOMA-IR) and Matsuda insulin sensitivity index (ISIM); β-cell function was assessed by disposition index (DI). We found that women with glucose intolerance had higher FAI levels compared to women with normal glucose tolerance (NGT) (prediabetes 6.2, T2DM 7.9 versus NGT 5.0, resp.; p < 0.001). Furthermore, there was a direct association between FAI levels and frequency of glucose intolerance (OR = 2.480, 95% CI 1.387–4.434), even after adjusting for age, BMI, waist circumference, hypertension, fasting insulin, testosterone, SHBG, and family history of diabetes. In addition, with FAI increase, glycosylated hemoglobin (HbA1c), plasma glucose concentrations, and serum insulin levels increased, while insulin sensitivity and β-cell function decreased. Our results suggested that androgen excess indicated by high FAI levels might serve as indicator of glucose intolerance, as it might promote insulin resistance and β-cell dysfunction in women with PCOS.

Sex hormone binding globulin, but not testosterone, is associated with the metabolic syndrome in overweight and obese women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with hyperandrogenism and an increased risk of Type 2 diabetes and cardiovascular disease. Decreased SHBG and elevated testosterone are associated with metabolic syndrome and glucose intolerance in women. The aim of this study was to assess the relationship between SHBG and testosterone and metabolic syndrome and glucose intolerance in PCOS. Cross-sectional study in overweight and obese premenopausal non-diabetic women with PCOS (no.=178: no.=55 metabolic syndrome, no.=16 glucose intolerance). Data were analyzed by multiple regression with metabolic syndrome, oral glucose tolerance test (OGTT) glucose or SHBG as dependent variables and reproductive hormones, insulin resistance, glucose tolerance, lipids or C-reactive protein as independent variables. Metabolic syndrome was independently associated with body mass index [odds ratio (OR) 1.084 95% confidence interval (CI) 1.034-1.170, p=0.015] and SHBG (OR 0.961 95% CI 0.932-0.995, p=0.018). Glucose tolerance was independently associated with OGTT insulin (β=0.418, p<0.001), age (β=0.154, p=0.033) and PRL (β=-0.210, p=0.002). SHBG was independently associated with OGTT insulin (β=-0.216, p=0.014) and PCOS diagnostic criteria (β=0.197, p=0.010). SHBG, but not testosterone, is independently associated with metabolic syndrome in overweight women with PCOS and is associated with insulin resistance and PCOS diagnostic criteria.

Impact of obstructive sleep apnea on insulin resistance and glucose tolerance in women with polycystic ovary syndrome.

Insulin resistance, impaired glucose tolerance, and type 2 diabetes are common in women with polycystic ovary syndrome (PCOS). Obstructive sleep apnea (OSA) has been linked to metabolic dysfunction. We studied women with and without PCOS to determine the extent to which OSA is responsible for insulin resistance and glucose intolerance in PCOS. In a prospective design, 52 women with PCOS and 21 women without PCOS of similar age and body mass index had an overnight polysomnogram and a 75-g oral glucose tolerance test. Twenty-nine women (56%) with PCOS had OSA compared with four controls (19%) (adjusted odds ratio 7.1; 95% confidence interval, 1.7-45.7; P = 0.01). PCOS women with OSA were more insulin resistant than those without OSA [homeostasis model assessment (HOMA) index 5.7 +/- 0.4 vs. 3.5 +/- 0.4; P = 0.006] after controlling for age, body mass index, and ethnicity. Impaired glucose tolerance was found in 16 of 29 (55%) PCOS women with OSA and only six of 23 (26%) of those without OSA (unadjusted P = 0.049). Insulin resistance and glucose intolerance were highly correlated with the presence and severity of OSA. Among PCOS women with normal glucose tolerance, the presence of OSA was associated with a nearly 2-fold higher fasting insulin level and HOMA index. The severity of OSA was a highly significant predictor of the fasting concentrations of glucose and insulin as well as the 2-h glucose concentration and HOMA index. OSA is a highly prevalent and important determinant of insulin resistance, glucose intolerance, and type 2 diabetes in PCOS.

Genetic contributions to glucose intolerance in polycystic ovary syndrome

Women with polycystic ovary syndrome (PCOS) are predisposed to develop impaired glucose tolerance and type-2 diabetes mellitus. Genetic factors appear to contribute to the insulin resistance that is characteristic of PCOS as well as to the failure of the pancreatic β-cell to compensate adequately for this insulin resistance. The cumulative results of studies examining the genetic contribution to both the reproductive and metabolic phenotypes of PCOS are consistent with PCOS as a complex, polygenic disorder. This article reviews the background and recent studies examining the genetic contributions to glucose intolerance in PCOS.

Assessment of glucose intolerance and insulin sensitivity in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is associated with increased risk of impaired glucose tolerance and type 2 diabetes. PCOS has been considered as a major risk factor for the development of diabetes, and screening of women with PCOS for glucose intolerance is suggested. Detection of glucose intolerance in PCOS is best performed via 2-h oral glucose tolerance test rather than fasting plasma glucose alone, since it enables diagnosis of both impaired glucose tolerance and diabetes. Insulin resistance is a prominent feature of PCOS, although not all women with PCOS have insulin resistance. Measurement of insulin resistance is not included in the diagnostic criteria of the syndrome, and not required for the selection of treatments in current clinical practice. However, this measurement is undoubtedly of great interest for clinical research studies of PCOS. Several methods are available to the clinical investigator for the measurement of insulin resistance, yet there is no universally accepted and clinically useful definition, and no specific guidelines about how to measure it. While hyperinsulinaemic glucose clamp is considered to be the ‘gold standard’ for the measurement of insulin resistance, several alternative methods have been validated against the gold standard. Each method has its own merits and disadvantages. The choice of method for a particular study should be based on the specific aims, size, and type of that study. Variability in measurement of insulin resistance due to physiological factors, assay-related problems, and protocol differences in dynamic function tests deserves much more emphasis when interpreting the results of a study, or making comparisons between studies.

7 Relation of functional ovarian hyperandrogenism to non-insulin dependent diabetes mellitus

Up to 40% of women with polycystic ovary syndrome (PCOS) demonstrate some degree of glucose intolerance, either impaired glucose tolerance (IGT) or non-insulin dependent diabetes mellitus (NIDDM). Defects in insulin action have long-been recognized as characteristic in these women. Recently, evidence has been obtained which documents that insulin secretory dysfunction also contributes significantly to the observed glucose intolerance. This chapter will focus on the recent evidence supporting the specific roles of disordered insulin secretion and action, in the development of glucose intolerance in PCOS. In addition, the use of pharmacological agents that modify insulin action as therapeutic options for women with PCOS, will be discussed.