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Fructose Consumption and Serum Uric Acid in Children with NASH

7/3/2017 4:15:41 PM
Nonalcoholic fatty liver disease (NAFLD), defined as the deposition of fat in the liver, is the hepatic manifestation of metabolic syndrome. NAFLD can progress over time to nonalcoholic steatohepatitis (NASH), which is a more severe condition that involves hepatic inflammation and fibrosis. NASH increases the risk for liver cirrhosis and liver cancer and can dramatically compromise quality of life. 
 
High consumption of dietary fructose, primarily in the form of sugary beverages, is thought to contribute to the pathogenesis of NAFLD by inducing de novo lipogenesis in the liver. Fructose is also rapidly metabolized in the liver via a biochemical pathway that consumes ATP to ultimately produce uric acid. Hyperuricemia is a feature of metabolic syndrome and NAFLD, and recent studies have shown that uric acid has the ability to stimulate production of inflammatory mediators.    
 
Given the associations between fructose consumption, hyperuricemia, and NAFLD as well as the potential risk of NAFLD to progress to NASH, researchers designed a study to test whether uric acid concentrations and fructose consumption are independently associated with NASH in children with proven NAFLD. The results of the study were published by Mosca et al. in the Journal of Hepatology (2017).
 
A total of 271 obese children and adolescents (mean age = 12.5yrs) with NAFLD underwent liver biopsy. Of these patients, 38% had NASH and 62% did not have NASH. After adjusting for known risk factors, fructose consumption was independently associated with NASH (OR=1.61; 95% CI, 1.25-1.86; p=.001). Serum uric acid concentration was also independently associated with NASH (OR=2.49; 95% CI, 1.87-2.83; p=.004). Finally, fructose consumption was independently associated with uric acid concentration (OR=2.02; 95% CI, 1.66-2.78; p=.01). 
 
The results of this study add to the growing body of evidence suggesting that fructose and uric acid contribute to the pathogenesis of NAFLD and its progression to NASH.
 
Reference: Mosca A, Nobili V, De Vito R, et al. Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents. J Hepatol. 2017;66(5):1031-1036.