Some adipokines, such as adiponectin and leptin, have been reported to be involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), while the association of adipsin and visfatin with NAFLD still remains unclear. This study aimed to examine the association of circulating adipsin, visfatin, and adiponectin with NAFLD in Chinese adults.
We recruited a total of 211 eligible subjects, including 100 NAFLD cases and 111 age and sex frequency-matched controls. Circulating adipsin, visfatin, and adiponection concentrations were measured by enzymatic immunoassay. Unconditional logistic regression was conducted to assess the associations between quartiles of adipokines and NAFLD.
Compared with the controls, NAFLD cases had higher levels of adipsin and lower levels of visfatin and adiponectin. By multivariate logistic analysis, adjusting for potential confounders, circulating adipsin levels were found to be positively associated with NAFLD risk, and circulating levels of visfatin and adiponectin were inversely associated with the risk of NAFLD (all p-trend < 0.05). The ORs were 3.76 (95% CI 1.27-11.08) for adipsin, 0.30 (95% CI 0.10-0.91) for visfatin, and 0.30 (95% CI 0.10-0.88) for adiponectin comparing subjects in the highest quartile with those in the lowest. After stratified by obesity status, the association of higher adipsin with increased risk of NAFLD was only observed in nonobese group. Additionally, the inverse association between adiponectin and NAFLD was found in both groups.
These results indicated that increased circulating levels of adipsin and decreased circulating levels of visfatin and adiponectin were independently associated with the increased risk of NAFLD.

Chronic airway inflammation is recognized as an essential process in the pathogenesis of asthma. Cytokine profiles derived from immune and inflammation cells such as T-helper (Th) cells, eosinophilia and neutrophilia are not limited to the Th2 type in asthma. However, little is understood about associations between Th2-low inflammatory cytokine profiles and risk of asthma in adults. A case-control study of 910 adult asthma and 881 healthy controls was conducted. Inflammatory cytokines screening was undertaken by high-throughput protein microarray technology, and Th17-related inflammatory cytokines (IL17A, IL-9, adipsin and CCL11) were finally selected. Associations between these four cytokines and adult asthma risk were analyzed by multivariate logistic regression models. We observed that plasma IL-17A and IL-9 levels were significantly increased in asthmatics when compared with controls. However, the plasma expressions of adipsin and CCL11 in asthmatics were significantly lower than that in health controls. The adjusted ORs (95%CI) of association between IL-17A, IL-9, adipsin and CCL11 expressions and adult asthma were 3.08 (1.91, 4.97), 1.93 (1.41, 2.64), 10.02 (6.99, 14.37) and 3.29 (2.36, 4.59), respectively (all P trend < 0.0001). Our results suggested that elevated IL-17A and IL-9 expressions and decreased levels of adipsin and CCL11 were positively associated with adult asthma.