In this cross-sectional study, we found that higher VAT rather than SAT increased risk for MA in men, and for women, the correlation of SAT only existed in BMI ≥ 24kg/m2. Higher VAT showed a significant positive association with MA in men and women, independent of BMI. VAT improved the predictive ability of MA comparing with BMI and WC. Deposit of abdominal adipose tissue associated with the risk of MA.
There are some differences between SAT and VAT in anatomical, cellular, molecular, physiological, clinical and so on(17). VAT has been considered the more pathogenic adipose tissue compartment compared with SAT(18). This may be related to the biological function of VAT, VAT was a metabolically active organ, which included more non-adipocytes including macrophages, immune cells, preadipocytes and fibroblasts, and could secrete amounts of inflammation mediators to induce metabolism impairments(17, 19–21). In addition, the high lipolytic activity of VAT and its accompanied inflammation response also contribute to abnormal lipogenesis, glucose homeostasis, and vascular health(22, 23). Therefore, it is plausible that higher VAT increased the risk for the metabolic abnormalities. With regards to the contribution of VAT in different sex, inconclusive results were reported(11, 12, 24–26). Several Caucasian population studies showed the associations of VAT with type 2 diabetes, hypertension and hyperlipidemia were stronger in women(11, 24, 27). In our supplemental table3(See Additional File 1), we observed that the effect of VAT on high TG and low-HDL were higher in men, indicating that VAT may have more striking effect on the lipid metabolism in men than women. Another possible reason was that only limited confounding factors were adjusted, which may have affected the results. Extending studies of the Chinese population needed to be expanded to determine gender differences in the contribution of VAT.
SAT is known to have adverse effects on a variety of metabolic risk factors and may have unique pathogenic properties independent of BMI (1, 7, 24, 28), and the effects of different levels of SAT on cardiometabolic factors are inconsistent(1, 7, 14, 18, 24, 29). In line with previous studies(29–31), our study (See Supplementary table 1 and 2, Additional File 1) showed higher SAT did not link to increased risk for hypertension, higher TG, and lower HDL-C independent of BMI, and SAT may be a protective factor for blood glucose. Several studies for European or African population found that SAT had independent associations with high blood pressure and HDL-C(1, 15, 25), suggesting the distinct effect of SAT across ethnics. A possible explanation for this gender difference in SAT was the distinct sex steroid hormone profiles since these sex hormones are important factors in regulating the adipose tissue distribution and energy metabolism(32, 33). For the protective effect of SAT, there were also several hypotheses to explain this observation. One is with smaller adipocyte, SAT was more insulin sensitive, and have a larger capacity to uptake fatty acids and triglycerides, thus can act as a powerful buffer to prevent excess fat into non-adipose tissue(34). On the other hand, SAT could secrete more favorable adipokines such as adiponectin, which had anti-diabetes and antiatherogenic properties(17, 22). Therefore, the different effects of SAT on metabolic outcomes may be related to its biological function.
Previous studies have shown that baseline and changes in VAT were independent predictors of future dyslipidemia, but BMI and SAT were not associated with future development of atherosclerotic dyslipidemia(35). The outcome was consistent to our study that VAT was a better indicator for predicting MA when compared to BMI and WC. Finally, VAT was more strongly associated with MA than BMI, WC, and SAT.
There are some advantages in our study. Areas of SAT and VAT were measured using MRI, which was the gold standard method of determining abdominal adipose tissue. The data, including anthropometric and questionnaire-based information, were collected by trained health professionals, and the biochemical measurements followed the standard protocols. Our study also has some limitations. First, we cannot infer causality between the fat indices and the metabolic abnormality because of the cross-sectional design. Second, limited confounding factors were included in this study, for example, regional fat distribution, such as deep SAT and superficial SAT, and drug use were not included, which may bias the results. Thirdly, the sample size of this study was relatively small. Finally, our data were based on only one single ethnic group, thus the results may not be applied to other ethnicities.