Research paper
Jensen T, Abdelmalek MF, Sullivan S, Nadeau KJ, Green M, Roncal C, Nakagawa T, Kuwabara M, Sato Y, Kang DH, Tolan DR, Sanchez-Lozada LG, Rosen HR, Lanaspa MA, Diehl AM, Johnson RJ. Fructose and sugar: A major mediator of non-alcoholic fatty liver disease. J Hepatol. 2018 May;68(5):1063-1075. doi:10.1016/j.jhep.2018.01.019
Why we cite it
Review article synthesizing evidence on how diets high in sugar (sucrose and/or HFCS) drive non-alcoholic fatty liver disease (NAFLD) and its inflammatory variant, non-alcoholic steatohepatitis (NASH). The central mechanism: fructose is metabolized by fructokinase C, which causes rapid ATP consumption and generates uric acid; the uric acid mediates hepatic fat accumulation through both increased de novo lipogenesis and impaired fatty acid oxidation. Fructose also increases gut permeability and alters the gut microbiome, contributing additional hepatic inflammation. These effects are distinct from those of glucose — fructose has unique metabolic properties that make it particularly hepatotoxic. The authors recommend reducing sugary beverages and total fructose intake, and note that blocking uric acid generation may provide therapeutic benefit. Part of the fructose cluster in the project alongside csf02, csf04, and csf05. Referenced by 1 companion and 1 companion-review.
DOI: 10.1016/j.jhep.2018.01.019 · PubMed 29408694 · Publisher