Of the 150 South Asians enrolled in the MASALA study, half of each sex, the average age was 57 ± 8 years and the average BMI was 26.1 ± 4.6 kg/m2. While BMI did not differ by sex, women had a higher percentage of body fat (40.7 ± 5.5% vs. 29.5 ± 6.0%, p < 0.001), higher amount of total body fat (26.4 ± 8.3 kg vs. 22.7 ± 7.5 kg, p < 0.01), and a higher amount of subcutaneous fat area by CT (287.0 ± 123.6 cm2 vs. 216.3 ± 89.0 cm2, p < 0.001). () However, men had a larger visceral fat area (155.6 ± 56.3 cm2 vs. 111.1 ± 47.8 cm2, p < 0.001, ) and a higher amount of hepatic fat (liver-to-spleen attenuation ratio of 1.2 ± 0.2 vs. 1.3 ± 0.3, p=0.04). Women had higher serum levels of both leptin (21.6 ± 11.6 vs. 9.1 ± 6.3 ng/ml, p < 0.01) and adiponectin (9.0 ± 5.8 vs. 5.7 ± 3.3 μg/ml, p < 0.01).
Differences in Body Composition Between Men and Women
In sex-stratified analyses, leptin was inversely associated with age among men only. In women, leptin was associated with HOMA-IR and triglycerides and showed a trend towards inverse association with HDL. In men, there was a similar trend towards association with HOMA-IR and inverse association with HDL. In both men and women, leptin was associated with metabolic syndrome but not with hypertension or diabetes. In women, leptin was strongly associated with all measures of both total and regional adiposity. In men, leptin was strongly associated with all measures of total adiposity and most measures of regional adiposity but not hepatic fat. ()
Sex-stratified characteristics of the MASALA participants by tertiles of leptin*
Adiponectin was associated with age in men but not in women. Furthermore, in women, adiponectin was associated with HDL, inversely associated with triglycerides and with HOMA-IR; whereas in men, adiponectin was inversely associated with triglycerides only. Adiponectin was not associated with diabetes, hypertension, or metabolic syndrome in either women or men. In women, adiponectin was not associated with any measures of total adiposity but was inversely associated with visceral fat and hepatic fat. On the other hand, adiponectin was not associated with any measure of body composition in men. () However, in combined analyses with both sexes, adiponectin was inversely associated with all measures of total and regional adiposity: BMI (p <0.001), percent body fat (p <0.001), total body fat (p <0.001), waist circumference (p <0.001), subcutaneous fat (p <0.01), visceral fat (p <0.001), and hepatic fat (p=0.01). (Data not shown.)
Sex-stratified characteristics of the MASALA participants by tertiles of adiponectin*
To further investigate the association between adipokines and adiposity, we conducted multivariate analyses adjusting for age, sex, smoking history, hypertension, HDL, triglycerides, and HOMA-IR in a stepwise manner. () After full adjustment, leptin remained strongly correlated to BMI, total body fat, and abdominal visceral fat (p < 0.001 for each), as well as hepatic fat (p=0.01). However, the inverse association between adiponectin and all body composition measures which we saw in our combined analyses no longer remained significant after adjusting for HDL and triglycerides; these metabolic covariates completely attenuated the association between adiponectin and BMI, total body fat, and hepatic fat. There remained a trend towards association between adiponectin and visceral fat after full adjustment. The associations between each adipokine and adiposity did not vary by sex (p-for-interaction >0.15 for each adiposity outcome with both leptin and adiponectin).
Sequentially adjusted associations between leptin (per 11 ng/ml)* and adiponectin (per 5 μg/ml)** and body fat composition measures
We conducted similar analyses to assess the association between high molecular weight adiponectin and body fat composition parameters. The results were essentially the same as those seen with total adiponectin; no significant association was seen after adjusting for covariates. (Data not shown.)
Lastly, we investigated the association between the adipokines and diabetes. In unadjusted models, leptin (per SD) was not associated with diabetes (OR 0.88, 95% CI 0.60–1.28, p=0.50). After adjusting for age, sex, hypertension, and smoking, there was a trend towards increased odds of diabetes with leptin (OR 1.48, 95% CI 0.91–2.42, p=0.12). Further adjusting for any measure of adiposity significantly attenuated this association. For adiponectin (per SD), there was a weak trend towards association with diabetes in unadjusted analyses (OR 0.73, 95% CI 0.47–1.14, p=0.17). After adjusting for age, sex, and hypertension, the association was further attenuated (OR 0.81, 95% CI 0.50–1.30, p=0.38). Adding any measure of adiposity further nullified the association. (Data not shown.)