Factors related with adiponectinemia in obese and normal-weight women and with its variation in weight loss programs

Objective: To assess different factors influencing adiponectinemia in obese and normal-weight women; to identify factors associated with the variation (Δ) in adiponectinemia in obese women following a 6-month weight loss program, according to surgical/non-surgical interventions. Methods: We studied 100 normal-weight women and 112 obese premenopausal women; none of them was on any medical treatment. Women were characterized for anthropometrics, daily macronutrient intake, smoking status, contraceptives use, adiponectin as well as IL-6 and TNF-α serum concentrations. Results: Adiponectinemia was lower in obese women (p < 0.001), revealing an inverse association with waist-to-hip ratio (p < 0.001; r = –0.335). Normal-weight women presented lower adiponectinemia among smokers (p = 0.041); body fat, waist-to-hip ratio, TNF-α levels, carbohydrate intake, and smoking all influence adiponectinemia (r 2 = 0.436). After weight loss interventions, a significant modification in macronutrient intake occurs followed by anthropometrics decrease (chiefly after bariatric procedures) and adiponectinemia increase (similar after surgical and non-surgical interventions). After bariatric intervention, Δ adiponectinemia was inversely correlated to Δ waist circumference and Δ carbohydrate intake (r 2 = 0.706). Conclusion: Anthropometrics, diet, smoking, and TNF-α levels all influence adiponectinemia in normal-weight women, although explaining less than 50% of it. In obese women, anthropometrics modestly explain adiponectinemia. Opposite to non-surgical interventions, after bariatric surgery adiponectinemia increase is largely explained by diet composition and anthropometric changes.

Insulin resistance does not play a major role in lipid and apolipoprotein profile in obese women

Background: Obesity is associated with increased atherogenesis through alterations in lipids, among other potential factors. Some of those abnormalities might be mediated by insulin resistance (IR). Aims: To compare lipid and apolipoprotein profile between lean and obese women; to evaluate the influence of IR on lipid and apolipoprotein profile, in obese women. Methods: We studied 112 obese and 100 normal-weight premenopausal women without known cardiovascular disease. Both groups were characterized for anthropometrics and a fasting blood sample was collected for assessment of glucose, insulin, triglycerides, cholesterol (total, LDL and HDL), and apolipoproteins A-I, A-II, B, C-II, C-III, and E; IR was assessed by the homeostatic model assessment (HOMA-IR). We compared lipids between obese and lean women; we looked for correlation of those levels with anthropometrics and IR (independently from anthropometrics) in obese women. Results: Obese women were characterized by mean age=34.6±8.3 years, BMI=43.6±7.9 kg/m2, waist circumference (Wc)=117.5±15.1 cm, and HOMA-IR=4.28±3.5. Lean women (age=34.2±8.3 years, BMI=21.4±1.7 kg/m2, Wc=71.7±5.8 cm, and HOMA-IR=1.21±0.76) presented with significantly lower levels of total cholesterol (P=0.001), LDL-cholesterol (P<0.001), and triglycerides (P<0.001); they presented higher levels of HDL-cholesterol (P<0.001), Apo A-I (P<0.001) and Apo A-II (P=0.037). HOMA-IR showed no significant association with apolipoproteins. HOMA-IR was inversely associated with HDL-cholesterol (P=0.048; r=−0.187) but that association disappeared when we adjusted for waist circumference. Only triglycerides were directly associated with HOMA-IR (P<0.001; r=0.343) independently from anthropometrics. Conclusion: We confirm that obese women present worst lipid and apolipoprotein profile. However, with the exception for triglycerides, insulin resistance per se does not play a major role in lipid and apolipoprotein abnormalities observed in obese women.