Introduction

Obesity, especially central obesity, is a well-established risk factor for a several diseases, such as dyslipidemia, type 2 diabetes (T2DM), cardiovascular diseases (CVD), and all-cause mortality [1, 10, 11, 25,26,27]. Several Caucasian studies have shown that VAT is more strongly associated with type 2 diabetes, hypertension and hyperlipidemia in female [10, 25, 28]. In our Additional file 1: Table S3, we observed that the effect of VAT on high TG and low-HDL was higher in male, indicating that VAT may have more striking effect on lipid metabolism in male than female. The possible reason maybe that only a limited number of confounders were adjusted, which may have affected the results. An expanded study of the Chinese population is necessary to determine the gender differences in the contribution of VAT. In general, the relationship between VAT and metabolic outcomes is relatively stable, which may be related to multiple biological effects 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, 6, 25, 29], and the effects of different levels of SAT on cardiometabolic factors are inconsistent [1, 6, 13, 19, 25, 30]. Consistent with previous studies [30,31,32], our study (See Additional file 1: Tables S1, S2) showed that higher SAT was not associated with hypertension, higher TG, and lower HDL-C risk after adjustment for age, smoke, drink, and menstrual history (for women), and SAT may be a protective factor for blood sugar. Several studies with European or African populations have found independent associations of SAT with high blood pressure (H-BP) and HDL-C [1, 14, 26], suggesting that SAT has different effects in different ethnic groups. A possible explanation for this sex difference in SAT is the different sex steroid hormone profiles, as these sex hormones are important in regulating adipose tissue distribution and energy metabolism [33, 34]. There are also several hypotheses for the protective effect of SAT to explain this observation. One is that smaller adipocytes, SAT are more sensitive to insulin and have a greater capacity to absorb fatty acids and triglycerides and therefore can act as a powerful buffer to prevent excess fat from entering non-adipose tissue [35]. On the other hand, SAT can secrete more favorable adipokines such as adiponectin, with antidiabetics and antiatherogenic properties [18, 23]. Therefore, the different effects of SAT on metabolic outcomes may be related to its biological functions. Since SAT has different effects on metabolic components in different sexes, it may result in a less stable correlation between SAT and metabolic abnormality.

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 [36]. This result is consistent to our study that VAT is a better predictor for MA compared with BMI and WC.

There are some advantages in our study. Areas of SAT and VAT were measured using MRI, which is the gold standard method of determining abdominal adipose tissue [37]. 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 a causal relationship between the adipose indices and the metabolic abnormality because of the cross-sectional design. Second, this study included limited confounding factors, such as not including regional fat distribution, such as deep SAT and superficial SAT, and medication use, which may have biased 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.

Conclusions

In male, VAT and SAT could increase the risk of metabolic abnormalities both at BMI < 24 kg/m2 and at BMI ≥ 24 kg/m2. In female, VAT could increase the risk of metabolic abnormalities but SAT could increase the risk of MA in the second and fourth quartiles (Q2 and Q4) only at BMI > 24 kg/m2. Deposition of abdominal adipose tissue was associated with metabolic abnormalities. VAT improved the predictive power of MA.