Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease
By T. Jensen, M. Abdelmalek, Shelby Sullivan, K. Nadeau, M. Green, Carlos Roncal, T. Nakagawa, M. Kuwabara, Yuka Sato, D. Kang and 6 more. Journal of Hepatology, 2018
805 citations recorded by the source corpus.
Nonalcoholic Fatty Liver Disease (NAFLD) is the hepatic manifestation of metabolic syndrome, and its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high fructose corn syrup (HFCS)) not only increases the risk for NAFLD, but also, nonalcoholic steatohepatitis (NASH). Here we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked with metabolism of fructose by fructokinase C, resulting in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations in gut permeability, microbiome, and associated endotoxemia contributes to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/df5d4f56c376d91a3e7171948b2642f1c697517c
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Citations in the corpus
- Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “Excessive consumption of fructose increases the incidence of obesity and nonalcoholic fatty liver disease (Hannou et al., 2018; Jensen et al., 2018).”
- Metabolomics for Investigating Physiological and Pathophysiological Processes. (2019, background): “Sugar-sweetened beverages with high fructose or sucrose levels also increase uric acid levels through the metabolism of fructose by fructokinase C, which increases ATP consumption as well as nucleotide turnover and hence uric acid generation (218).”