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 mechanism it proposes, under its own ”Recent evidence suggests”: fructose metabolised by fructokinase C consumes ATP and generates uric acid, which mediate fat accumulation, and the review attributes that accumulation to both increased lipogenesis and impaired fat oxidation. Alterations in gut permeability, the microbiome and endotoxemia are named as contributing to the risk of NAFLD and NASH. The review places ”the unique aspect of fructose metabolism” in its first two enzymatic steps, where it differs from glucose. On practice it is hedged twice: ”Early clinical studies suggest” that reducing sugary beverages and total fructose intake ”may have a significant benefit”, and the authors call for ”larger, more definitive trials” of lowering sugar intake and of blocking uric acid generation.
DOI: 10.1016/j.jhep.2018.01.019 · PubMed 29408694 · Publisher
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