title: 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.
authors.affiliation: Department of Gynecology and Obstetrics, Aarhus Kommunehospital, Denmark.
authors.forename: P
authors.initials: P
authors.lastname: Ovesen
authors.forename: J
authors.initials: J
authors.lastname: Moller
authors.forename: H J
authors.initials: HJ
authors.lastname: Ingerslev
authors.forename: J O
authors.initials: JO
authors.lastname: Jørgensen
authors.forename: A
authors.initials: A
authors.lastname: Mengel
authors.forename: O
authors.initials: O
authors.lastname: Schmitz
authors.forename: K G
authors.initials: KG
authors.lastname: Alberti
authors.forename: N
authors.initials: N
authors.lastname: Moller
mesh_terms: D000328:Adult; D001835:Body Weight; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D007333:Insulin Resistance; D050356:Lipid Metabolism; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*
chemical_list: D007328:Insulin; D005947:Glucose