This study was the first report to examine the serum concentration of asprosin in MetS subjects. The main findings were as follows: i) serum asprosin levels were markedly increased in MetS patients than in healthy controls, and showed an increasing trend with the increased numbers of metabolic components; ii) serum asprosin levels were positively correlated with BMI, WC, Fat%, FPG, 2 h-PG, FIns, HOMA-IR, TG, MCP-1 and IL-6, and negatively correlated with HDL cholesterol; iii) serum asprosin was independently and positively correlated with the occurrence of MetS and IR even after controlling for the covariates.
Asprosin has recently been identified as a white tissue-derived novel adipokine and its concentrations have been confirmed to be increased in adults with T2DM and PCOS [11–13]. However, the information remains unavailable regarding the role of asprosin in MetS. Here, we showed that serum asprosin levels were markedly elevated in MetS, which was similar to a recent study conducted in patients with T2DM [11, 12]. Nevertheless, the reason for the increase of asprosin secretion is unknown. Previous studies have demonstrated that plasma asprosin was pathologically elevated in mice and humans with IR, while asprosin-specific monoclonal antibody lowered plasma asprosin and improved insulin sensitivity in these mice [8, 9]. Hence, we speculate that asprosin may serve as a risk factor associated with the pathogenesis of MetS. However, the cross-sectional nature of the current study still can’t rule out the possibility that the elevation of serum asprosin in MetS might be a compensatory up-regulation for counteracting the metabolic stress produced by adiposity, hyperglycemia, or hyperlipidemia. Therefore, a follow up study will be necessary.
IR is generally considered to be a root causative factor for developing MetS. Adipose tissue has the endocrine role to regulate energy balance and glucose homeostasis. Several adipose tissue-secreted cytokines can either enhance or impair insulin action . Data for the current study clearly showed that asprosin was significantly positively correlated with the well-known indices of MetS in all individuals. Among these indices, HOMA-IR was independent related factors with serum asprosin levels. Previous studies have found that intraperitoneal injection of asprosin antibody can significantly reduce serum insulin levels and improve IR in obese mice . Two recent clinical studies have also found that circulating asprosin concentrations are positively correlated with IR in patients with T2DM or PCOS [11, 13]. It is suggested that the correlation between asprosin and MetS may be part attributed to IR. In addition, the ROC curve analysis showed that serum asprosin might be a useful marker for the prediction of MetS and IR in our study population. In one aspect, the value of AUC (0.712) and (0.742) was considered to be moderate significance, which may be due to the relatively small sample size and a non-normal distribution in the studied population. In another aspect, the serum asprosin may be not an ideal marker for predicting MetS and IR.
Dyslipidemia and hyperglycemia are the pathological state characterized of MetS and play crucial parts in the pathogenesis of the disease . Our data demonstrates that serum asprosin levels are significantly correlated with TG, HDL-C, FBG, and 2 h-PBG even after adjustment for age and BMI. Our multiple stepwise regression analysis has identified the TG as significant independent contributors to circulating asprosin levels. These findings raise the hypothesis that asprosin may provide a molecular association between glucose - lipid metabolism and MetS. Although it would be premature to conclude the causal effects of asprosin on these parameters, it would be of interest to explore whether therapeutically targeting asprosin may ameliorate metabolic disorder in MetS subjects.
Chronic low-grade inflammation is closely related to obesity and IR and can lead to the pathogenesis of some metabolic-related diseases. Previous study demonstrated that asprosin promotes hepatic glucose production by activating cAMP second - messenger system, which was also involved in the inflammatory response . Another in vitro experiment displayed that siRNA-mediated asprosin suppression improved NF-κB phosphorylation and release of TNF-α and MCP-1 in the palmitic- treated pancreatic cells . However, a recent clinical research showed that serum asprosin had no significant association with the hs-CRP in diabetic patients, which function as an acute inflamatory marker of inflammation . These controversial results prompted us to further explore the association between asprosin and metabolic inflammation. Thus, we measured the inflammatory marker IL-6 and MCP-1 level in all subjects and found that even after adjusting for age and BMI factors, asprosin did find a significant correlation with IL-6. Further studies are still needed to clarify the precise function asprosin in metabolic inflammation.
This study also has certain limitations. Firstly, it is difficult to deduce the causal relationship between serum asprosin levels and MetS due to the cross-sectional study design. Hence, a larger sample of prospective studies needs to be confirmed. Secondly, the study is based on the Chinese population and therefore needs to be carefully promoted to other ethnic groups. Thirdly, related inflammation indicators such as hs-CRP were not tested. Fourth, our study only detects serum levels based on ELISA, and there may be some random measurement errors.