The role of LCPUFA-ω3 on the obesity-associated hyperandrogenemia of pubertal girls: secondary analysis of a randomized clinical trial.

Introduction Hyperandrogenism (HA), either clinical or biochemical, is associated with obesity in adolescent girls. Long chain polyunsaturated fatty acids ω3 (LCPUFA-ω3) play protective roles in some obesity-associated morbidities, but their contribution to preventing HA is unclear. Our aim was to examine the potential positive relationships between erythrocyte LCPUFA-ω3, with or without supplementation, and hyperandrogenemia. Methods Secondary analysis of a clinical trial that was conducted previously to analyze the effect of LCPUFA-ω3 on insulin resistance and body weight. Here, we present a cross-sectional analysis of 180 girls with obesity, and a longitudinal analysis of 117 girls who completed a 3-month supplementation period (57 LCPUFA-ω3 [DO3] and 60 placebo [DP)]). Dehydroepiandrosterone sulfate (DHEAS), total testosterone (TT) and steroid hormone binding globulin (SHBG) were measured with chemiluminescence; free testosterone (FT) was calculated. Erythrocyte fatty acids were determined by gas chromatography. Non-parametric statistics was used for analysis. Results In cross-sectional analysis, age (odds ratio [OR] = 1.35; 95% confidence interval [CI] = 1.03, 1.78; p = 0.027), insulin (OR = 1.05; 95% CI: 1.00, 1.10; p = 0.018), and erythrocytes eicosapentaenoic acid (EPA) (OR = 0.04; 95% CI: 0.01, 0.65; p = 0.012) were predictors of hyperandrogenemia (FT >0.63 ng/mL). In longitudinal analysis, EPA, adiponectin and SHBG increased, while FT decreased, in the DO3 group (p < 0.05). The risk of hyperandrogenemia at the end of follow-up was predicted by basal hyperandrogenemia (OR = 18.16, 95% CI: 5.37, 61.4; p < 0.001) and by increases in EPA (OR = 0.40; 95% CI: 0.01, 0.65; p = 0.06 marginal significance). Conclusions Our results suggest a preventive role of EPA on the risk for hyperandrogenemia in girls with obesity, but further studies are needed to demonstrate a benefit.

Obesity Is Associated with Changes in Iron Nutrition Status and Its Homeostatic Regulation in Pregnancy.

The influence of obesity on maternal iron homeostasis and nutrition status during pregnancy remains only partially clarified. Our study objectives were (1) to describe how obesity influences broad iron nutrition spectrum biomarkers such as available or circulating iron (serum transferrin receptor (sTfr) and serum iron), iron reserves (ferritin), and functional iron (hemoglobin); and (2) to depict the regulating role of hepcidin. The above was carried out while considering influential factors such as initial iron nutrition status, iron intake, and the presence of inflammation. Ninety three non-anemic pregnant adult women were included, 40 with obesity (Ob) and 53 with adequate weight (AW); all took ≈30 mg/day of supplementary iron. Information on iron intake and blood samples were obtained at gestational weeks 13, 20, 27, and 35. A series of repeated measure analyses were performed using General Linear Models to discern the effect of obesity on each iron indicator; iron intake, hepcidin, and C-reactive protein were successively introduced as covariates. Available and circulating iron was lower in obese women: sTfr was higher (p = 0.07) and serum iron was lower (p = 0.01); and ferritin and hemoglobin were not different between groups. Hepcidin was higher in the Ob group (p = 0.01) and was a significant predictor variable for all biomarkers. Obesity during pregnancy dysregulates iron homeostasis, resembling "obesity hypoferremia".