Serum uric acid is independently and linearly associated with risk of nonalcoholic fatty liver disease in obese Chinese adults

被引:31
|
作者
Liu, Chang-Qin [1 ]
He, Chun-Mei [2 ]
Chen, Ning [1 ]
Wang, Dongmei [3 ]
Shi, Xiulin [1 ]
Liu, Yongwen [1 ]
Zeng, Xin [2 ]
Yan, Bing [2 ]
Liu, Suhuan [2 ]
Yang, Shuyu [1 ,2 ]
Li, Xiaoying [1 ,2 ,4 ]
Li, Xuejun [1 ,2 ]
Li, Zhibin [2 ,3 ,5 ]
机构
[1] Xiamen Univ, Affiliated Hosp 1, Dept Endocrinol & Diabet, Xiamen, Peoples R China
[2] Xiamen Diabet Inst, Xiamen, Peoples R China
[3] Xiamen Univ, Sch Publ Hlth, Xiamen, Peoples R China
[4] Fudan Univ, Zhongshan Hosp, Dept Endocrinol, Shanghai, Peoples R China
[5] Xiamen Univ, Affiliated Hosp 1, Epidemiol Res Unit, Xiamen, Peoples R China
来源
SCIENTIFIC REPORTS | 2016年 / 6卷
关键词
METABOLIC SYNDROME; INSULIN-RESISTANCE; UNITED-STATES; POPULATION; PREVALENCE; PREDICTORS; REGRESSION; IRISIN; IMPACT;
D O I
10.1038/srep38605
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The present study aimed to explore the independent association and potential pathways between serum uric acid (SUA) and nonalcoholic fatty liver disease (NAFLD). 1365 community-living obese Chinese adults who received hepatic ultrasonography scanning were included. The prevalence rates of NAFLD were 71.5% for men and 53.8% for women. Compared with controls, NAFLD subjects showed significantly increased SUA levels (333.3 +/- 84.9 v.s. 383.4 +/- 93.7 mu mol/L) and prevalence rate of hyperuricemia (HUA) (25.7% v.s. 47.3%, p < 0.001). After adjustment for insulin resistance (IR), components of metabolic syndrome (MetS) and other potential confounders, elevated SUA is independently associated with increased risk of NAFLD, with the adjusted OR of 1.528-2.031 (p < 0.001). By using multivariable fractional polynomial (MFP) modeling, the best FP transformation model shows that SUA was independently and linearly associated with risk of NAFLD. The one-pathway model by using structural equation modeling (SEM) about the relationships among SUA, IR, components of metabolic syndrome and NAFLD fits well (chi(2) = 57.367, p < 0.001; CFI = 0.998; TLI = 0.992; and RMSEA = 0.048) and shows SUA might increase the risk of NAFLD directly besides of the indirect effects through increasing fasting insulin, blood pressure, triglyceride and decreasing HDL-C levels. Our results imply that elevated SUA may play an important role in NAFLD pathogenesis.
引用
收藏
页数:10
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