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Context: Polycystic ovarian syndrome (PCOS) is often associated with obesity and diabetes. Objective: The present study measured body fat distribution and metabolic risk factors in women with features of PCOS. Design: Cross-sectional, multiethnic study of cardiovascular risks. Setting: General community. Study Participants: 145 PCOS and 344 non-PCOS women. Exposure Measures: Body composition by dual x-ray absorptiometry; abdominal fat masses measured by magnetic resonance imaging and hepatic triglyceride by magnetic resonance spectroscopy. Outcomes Measures: Body composition, liver fat content, homeostatic model assessment for insulin resistance (HOMA-IR), revised, and metabolic syndrome components. Results: PCOS women had a higher free androgen index compared with the non-PCOS women. Nonobese PCOS and non-PCOS women had a similar body fat content and distribution, HOMA-IR, and hepatic triglyceride content. Obese PCOS women had a similar total body fat percentage compared with their non-PCOS counterparts (41.4% and 41.4% respectively). Both obese groups had similar intraperitoneal fat (1.4% of total body mass in PCOS vs 1.4% in non-PCOS). However, obese PCOS women had a greater ratio of truncal/lower body fat (1.42 vs 1.27; P < 0.016). They also had greater insulin resistance (HOMA-IR: PCOS, 2.24% vs non-PCOS, 1.91%; P < 0.016), higher liver triglyceride content (6.96% in PCOS vs 4.44% in non-PCOS; P < 0.016), and a greater incidence of hypertension (33% vs 24%; P < 0.05). No differences were observed in other metabolic risk factors. Conclusions: Both obese and nonobese women with PCOS features had a greater free androgen index compared with non-PCOS women, but neither had greater intraperitoneal fat or abnormal lipid levels. Obese, but not nonobese, women with PCOS had a greater truncal/lower extremity fat ratio, HOMA-IR, and liver triglyceride content., Obese and non-obese PCOS women have a higher free androgen index than do non-PCOS women. Neither have high intraperitoneal fat. Only obese PCOS women have higher upper body fat, HOMA-IR, and liver fat content.

Obesity and diabetes are more common in African-Americans than whites. Because free fatty acids (FFA) participate in the development of these conditions, studying race differences in the regulation of FFA and glucose by insulin is essential.The objective of the study was to determine whether race differences exist in glucose and FFA response to insulin.This was a cross-sectional study.The study was conducted at a clinical research center.Thirty-four premenopausal women (17 African-Americans, 17 whites) matched for age [36 ± 10 yr (mean ± sd)] and body mass index (30.0 ± 6.7 kg/m²).Insulin-modified frequently sampled iv glucose tolerance tests were performed with data analyzed by separate minimal models for glucose and FFA.Glucose measures were insulin sensitivity index (S(I)) and acute insulin response to glucose (AIRg). FFA measures were FFA clearance rate (c(f)).Body mass index was similar but fat mass was higher in African-Americans than whites (P0.01). Compared with whites, African-Americans had lower S(I) (3.71 ± 1.55 vs. 5.23 ± 2.74 [×10⁻⁴ min⁻¹/(microunits per milliliter)] (P = 0.05) and higher AIRg (642 ± 379 vs. 263 ± 206 mU/liter⁻¹ · min, P0.01). Adjusting for fat mass, African-Americans had higher FFA clearance, c(f) (0.13 ± 0.06 vs. 0.08 ± 0.05 min⁻¹, P0.01). After adjusting for AIRg, the race difference in c(f) was no longer present (P = 0.51). For all women, the relationship between c(f) and AIRg was significant (r = 0.64, P0.01), but the relationship between c(f) and S(I) was not (r = -0.07, P = 0.71). The same pattern persisted when the two groups were studied separately.African-American women were more insulin resistant than white women, yet they had greater FFA clearance. Acutely higher insulin concentrations in African-American women accounted for higher FFA clearance.

Background: C-reactive protein (CRP) levels are significantly influenced by adiposity and are higher in women compared with men. We postulated that there may be sex differences in the relationship between CRP and body fat. Methods: We measured CRP and body fat parameters in 1166 men and 1413 women ages 30–65 in the population-based Dallas Heart Study. Total fat mass (TFM) was measured using dual-energy x-ray absorptiometry scanning and was subdivided into truncal fat (TrF) and lower body fat (LBF). The TrF/LBF ratio was used to measure fat distribution. Abdominal fat compartments (ip and sc) were measured using magnetic resonance imaging. Log-transformed CRP was used as the outcome variable in sex-combined models with interaction tests. Results: Median body mass index was higher in women than in men (29.9 vs. 28.2 kg/m2), as was TFM (29.7 vs. 20.5 kg) (P < 0.001 each). TFM was linearly associated with log CRP in both sexes, with a steeper slope of association in women (P interaction = 0.003). CRP increased to a greater degree with increasing TrF (P interaction = 0.0004) in women compared with men, even after adjustment for TFM; values were similar across sexes for LBF. Fat distribution (TrF/LBF ratio) was more strongly associated with CRP levels in women vs. men (R2 adjusted for TFM = 0.04 vs. 0.008). Greater increases in CRP were also observed with increasing ip and sc fat in women compared with men. Conclusions: The quantity and distribution of body fat influence CRP to a greater extent in women compared with men. Adiposity as a contributor to subclinical inflammation may be particularly relevant in women.

Objectives: Several reports indicate that the body fat compartments, especially ip fat, predict metabolic risk better than total body fat. The objective of the study was to determine whether this can be confirmed and generalized throughout the population.Participants: A representative sample of 1934 Black and White women and men of the Dallas Heart Study participated in the study.Design: We measured the fat in total body, trunk, and lower body with dual-energy x-ray absorptiometry and in abdominal compartments (sc, ip, and retroperitoneal) with magnetic resonance imaging. Other measurements included body mass index (BMI), waist circumference, blood pressure, plasma lipids, glucose, insulin (including homeostasis model), and C-reactive protein.Results: In all groups, total body fat correlated positively with key metabolic risk factors, i.e. homeostasis model, triglyceride/high-density lipoprotein-cholesterol ratios, C-reactive protein, and blood pressure; however, it explained less than one third of the variability of all the risk factors. After adjustment for total body fat, truncal fat conferred additional positive correlation with risk factors. Furthermore, with multivariable regression analysis, ip fat conferred independent correlation with plasma lipids beyond a combination of other compartments including truncal fat. Still, except for insulin levels, all combinations including ip fat still explained less than one third of the variability in risk-factor levels. Conversely, lower body fat correlated negatively with risk factors; i.e. lower body fat appeared to offer some protection against risk factors.Conclusions: Body fat distribution has some influence on risk factors beyond total body fat content. Both waist circumference and BMI significantly predicted risk factors after adjustment for total body fat, and for clinical purposes, most of the predictive power for men was contained in waist circumference, whereas for women, BMI and waist circumference were similarly predictive. Finally, even though the correlations between combined body fat parameters and risk factors explained only a portion of the variation in the latter, the average number of categorical metabolic risk factors increased progressively with increasing obesity. Hence, obesity seemingly has more clinical impact than revealed in these correlative studies.