Normal basal and insulin-stimulated fuel metabolism in lean women with the polycystic ovary syndrome.

Abstract

Many reports have suggested that hyperandrogenaemic patients with the polycystic ovary syndrome (PCOS) may be insulin resistant. However, there have also been suggestions that their insulin resistance may relate to obesity and android fat distribution. To assess whether PCOS induces metabolic disturbances independently of obesity, we studied seven lean patients with PCOS (age, 27.1 +/- 2.0 yr; body mass index, 22.2 +/- 0.78 kg/m2; waist/hip ratio, 0.79 +/- 0.02; fat-free mass, 46.38 +/- 1.13 kg) and seven normal women (age, 25.7 +/- 1.4 yr; body mass index, 21.3 +/- 0.69 kg/m2; waist/hip ratio, 0.74 +/- 0.02; fat-free mass, 50.1 +/- 1.51 kg) for 3 h in the basal period and 2 h during a hyperinsulinemic (0.4 mU/kg.min) euglycemic clamp. In the basal state, comparable metabolic indices were recorded: serum insulin, 35.9 +/- 7.7 (PCOS) vs. 37.3 +/- 2.87 pmol/L (controls); plasma C-peptide, 364.1 +/- 66.2 vs. 397.2 +/- 66.2 pmol/L; plasma glucose, 4.95 +/- 0.09 vs. 4.77 +/- 0.09 mmol/L; forearm arterio-venous difference in glucose, 0.17 +/- 0.04 vs. 0.15 +/- 0.07 mmol/L; isotopically determined endogenous glucose production, 1.9 +/- 0.1 vs. 2.0 +/- 0.1 mg/kg.min; and serum nonesterified fatty acids, 545 +/- 40 vs. 617 +/- 54 mumol/L (all P > 0.05). During the clamp, all recordings were again similar: serum insulin, 282.7 +/- 21.5 vs. 270.5 +/- 13.6 pmol/L; plasma C-peptide, 331.0 +/- 33.1 vs. 364.1 +/- 66.2 pmol/L; plasma glucose, 4.99 +/- 0.07 vs. 4.99 +/- 0.05 mmol/L; glucose arterio-venous difference, 1.01 +/- 0.18 vs. 0.85 +/- 0.12 mmol/L; endogenous glucose production, -0.9 +/- 0.1 vs. -0.5 +/- 0.2 mg/kg.min; amount of exogenous glucose necessary to maintain euglycemia, 4.0 +/- 0.4 vs. 3.8 +/- 0.5 mg/kg.min; and nonesterified fatty acids, 205 +/- 7 vs. 246 +/- 18 mumol/L (all P > 0.05). By showing normal basal and insulin-stimulated substrate metabolism in lean hyperandrogenemic PCOS patients, these data suggest that insulin resistance may be an epiphenomenon, rather than a primary feature of PCOS.

The insulin-resistant phenotype of polycystic ovary syndrome

“…However, prevalence data on IR in PCOS are inconsistent and influenced by multiple factors including study population, evaluation methods of insulin sensitivity, BMI, family history of diabetes, and diagnostic criteria for PCOS (31,(36)(37)(38)(39)(40). In particular there has been some incongruent results regarding the lean group of women with PCOS, who may not be as insulin resistant as the obese counterpart, but may be more insulin resistant than lean women without PCOS (38). Results on this issue may also be hampered by the use of many different phenotypes of PCOS, which may, not all, be predictors of IR.…”

Scientific Statement on the Diagnostic Criteria, Epidemiology, Pathophysiology, and Molecular Genetics of Polycystic Ovary Syndrome

“…And whereas obesity increases insulin resistance, lean women with PCOS have the same level of insulin sensitivity as obese controls (99, 104, 283), or in some cases lean controls (284,285). The reason for not detecting differences in insulin sensitivity in lean women with PCOS might be explained by racial/ethnic differences, and this warrants further investigation (286,287). Women with 1990 NIH-defined PCOS, which includes HA, have greater insulin resistance compared to anovulatory women with PCOS who have normal androgen levels and are relatively healthier metabolically (288 -290), whereas a relatively normal weight (BMI Ͻ 27 kg/m 2 ) significantly ameliorates this metabolic risk (134,291).…”

The prevalence and risk factors for glucose intolerance in young Korean women with polycystic ovary syndrome

“…Several studies using the euglycemic hyperinsulinemic clamp showed that insulin resistance was consistently present in obese PCOS women, however, the results have been conflicting in lean women with PCOS [8][9][10][11][12][13]. Moreover, the role of insulin resistance as a risk factor for the development of glucose intolerance has still not been clearly defined in women with PCOS.…”