Impaired ApoB-Lipoprotein and Triglyceride Metabolism in Obese Adolescents with Polycystic Ovary Syndrome.

CONTEXT: Adolescents with polycystic ovary syndrome (PCOS) have atherogenic dyslipidemia and increased cardiovascular disease (CVD) risk, and this is exacerbated in obesity. OBJECTIVE: To determine and compare fasting and nonfasting lipid and apolipoprotein (Apo)B-lipoprotein metabolism in 3 groups of adolescent girls: healthy-weight controls, obese without PCOS (obese-control), and obese with PCOS (obese-PCOS). DESIGN, SETTING, AND PARTICIPANTS: Participants aged 12 to 17 years were recruited for this cross-sectional study from a pediatric weight management clinic and the local community in Alberta, Canada. MAIN OUTCOME MEASURES: Plasma lipids and ApoB lipoproteins, including triglycerides (TGs) and ApoB100- and ApoB48-lipoproteins, were measured in the fasted and postprandial state following a high-fat meal. RESULTS: Obese-control (n = 12) and obese-PCOS (n = 18) groups had twofold higher concentrations of fasting plasma TG and ApoB100- and ApoB48-lipoprotein remnants compared to healthy-weight controls (n = 10) (ApoB48-lipoproteins: 19.32 ± 2.10, 24.02 ± 4.28, and 8.95 ± 1.05 μg/mL, respectively; P < 0.001). The obese-PCOS group had 50% higher fasting plasma TG level compared to the obese-control group. The postprandial response was higher in both obese-controls and obese-PCOS subjects compared with healthy-weight controls in plasma TG area under the curve (AUC) (1028.0 ± 83.67, 1587.01 ± 259.6, and 615.42 ± 76.42 μg/mL⋅h, respectively; P < 0.01) and ApoB48(AUC) (191.30 ± 19.06, 238.8 ± 37.73, and 96.58 ± 9.17 μg/mL⋅h, respectively; P < 0.0001). Nonfasting plasma TG(AUC) and ApoB48(AUC) were positively correlated with free testosterone (r = 0.38; P < 0.001 and r = 0.33; P < 0.05, respectively), and these relationships were highly associated with insulin and body mass index. CONCLUSIONS: Adolescent girls with obesity and PCOS have elevated fasting and postprandial plasma TG and ApoB-lipoprotein remnants, providing evidence of early subclinical CVD risk, and these indices are highly associated with impaired insulin metabolism and hyperandrogenemia.