Dataset Information

No Evidence for a Causal Link between Serum Uric Acid and Nonalcoholic Fatty Liver Disease from the Dongfeng-Tongji Cohort Study.

ABSTRACT:

Background and aims

Elevated serum uric acid (SUA) is associated with an increased risk of nonalcoholic fatty liver disease (NAFLD); however, whether this association is causal is undetermined.

Methods

Each participant from the Dongfeng-Tongji cohort study based on 27,009 retirees was interviewed face-to-face following a clinical examination. Covariance, logistic regression analysis, and instrumental variables were used to assess associations between SUA and (severity of) NAFLD and the causal link.

Results

Among 8,429 subjects free of NAFLD at baseline, 2,007 participants developed NAFLD after 5 years of follow-up. The multivariable-adjusted odds ratio (OR) for NAFLD for individuals in the fourth quartile of SUA level versus those in the first was 1.71 (95% CI: 1.45-2.01, P for trend <0.001) and was more dramatic in women or normal-weight persons. Furthermore, SUA was materially associated with greater mean markers of hepatic necroinflammation and greater probabilities of fibrosis. In genetic analyses, both single nucleotide polymorphisms (rs11722228 to SLC2A9 and rs2231142 to ABCG2) were pronouncedly associated with increased SUA concentrations, ranging from 0.19 to 0.22 mg/dl. No significant associations were observed between SNPs and potential confounders. No association was observed between the SUA-increasing allele and NAFLD, with an OR of 0.98 (95% CI: 0.90-1.08) per genetic score. This was not significantly different (P = 0.25) from what was expected (1.03, 95% CI: 1.03-1.03).

Conclusions

SUA was positively associated with NAFLD incidence especially in female and normal-weight individuals and the suspected progression risk of newly developed NAFLD. However, the Mendelian randomization analyses lend no causal evidence, suggesting high SUA as a marker and not a cause of NAFLD.

SUBMITTER: Tang Y

PROVIDER: S-EPMC8941576 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Publications

No Evidence for a Causal Link between Serum Uric Acid and Nonalcoholic Fatty Liver Disease from the Dongfeng-Tongji Cohort Study.

Tang Yuhan Y Xu Yanyan Y Liu Peiyi P Liu Cheng C Zhong Rong R Yu Xiao X Xiao Lin L Du Min M Yang Ling L Yuan Jing J Wang Youjie Y Chen Weihong W Wei Sheng S Liang Yuan Y Zhang Xiaomin X Wu Tangchun T He Meian M Miao Xiaoping X Yao Ping P

Oxidative medicine and cellular longevity 20220315

<h4>Background and aims</h4>Elevated serum uric acid (SUA) is associated with an increased risk of nonalcoholic fatty liver disease (NAFLD); however, whether this association is causal is undetermined.<h4>Methods</h4>Each participant from the Dongfeng-Tongji cohort study based on 27,009 retirees was interviewed face-to-face following a clinical examination. Covariance, logistic regression analysis, and instrumental variables were used to assess associations between SUA and (severity of) NAFLD an ...[more]

PMID: 35340212

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Project description:Background & aimsNonalcoholic fatty liver disease (NAFLD) has multifactorial origin. Genetic and environmental factors lead to the biology of this complex disorder. In this study, we screened parents of cases with NAFLD and compared them with parents of cases without NAFLD to see its familial aggregation and the role of patatin-like phospholipase domain containing 3 (PNPLA3).MethodIt was a cross-sectional study. Parents of probands with NAFLD and without NAFLD were screened with abdominal sonography, anthropometry, blood tests, transient elastography, and PNPLA3 polymorphism.ResultsWe had enrolled 303 individuals: 51 probands with NAFLD, 50 probands without NAFLD, and their 202 parents. Parents of the NAFLD group had significantly higher metabolic risk factors as compared with parents of the non-NAFLD group. They had a significantly higher rate of fatty liver (P = 0.0001), mean serum aspartate aminotransferase levels (P = 0.011), mean serum alanine aminotransferase levels (P = 0.001),raised fasting and postprandial blood sugar levels, lower mean platelets (P = 0.033) and serum albumin levels (P = 0.005), and higher mean liver stiffness (P = 0.001) on transient elastography.Frequency of PNPLA3 polymorphism within NAFLD group was higher compared to the non-NAFLD group (mutant GG-13.3 vs 3.3%). Similarly, parents of NAFLD group had mutant GG in 15 % versus 5% in parents of non-NAFLD group, (P = 0.105, odds ratio 6), though it was not statistically significant but may be relevant. In this study, offsprings of parents with nonalcoholic steatohepatitis were likely to have GG homozygous allele. A NAFLD16 score based on parent's parameters was calculated to predict the probability of NAFLD occurrence in an overweight obese individual.ConclusionScreening of parents of individuals with NAFLD will help in the identification of undiagnosed NAFLD cases and other metabolic risk factors among them as there is a familial aggregation of NAFLD. One can predict the occurrence of NAFLD in the next generation using the NAFLD16 score.

Dataset Information

No Evidence for a Causal Link between Serum Uric Acid and Nonalcoholic Fatty Liver Disease from the Dongfeng-Tongji Cohort Study.

Background and aims

Methods

Results

Conclusions

Publications

No Evidence for a Causal Link between Serum Uric Acid and Nonalcoholic Fatty Liver Disease from the Dongfeng-Tongji Cohort Study.

Similar Datasets

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