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 — Jensen T, Abdelmalek MF, Sullivan S, et al.

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Objective

  • To review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation.

Background

  • Historically thought to result from over-nutrition and a sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high fructose corn syrup [HFCS]) not only increase the risk of NAFLD, but also non-alcoholic steatohepatitis (NASH).
  • However, metabolic studies indicated that the amount of fructose being converted to triglycerides was relatively small and do not account for the lipogenic response observed. This led some scientists to question the importance of fructose as a means of stimulating lipid synthesis and accumulation.
  • Still, the importance of fructose reemerged with reports linking intake of sugar-sweetened beverages, and in particular fructose, with non-alcoholic fatty liver disease (NAFLD), an association that has been confirmed in numerous other studies and is now a major area of research.

Methods

  • Details of the methods utilized in the selection of studies for this review were not provided in this article.

Findings

  • The majority of evidence suggests that fructose worsens lipid profiles and insulin sensitivity, likely contributing to the development of NAFLD.
  • Experimental studies indicate that that fructose-induced metabolic syndrome could be partially inhibited by treatment with allopurinol, a xanthine oxidase inhibitor that blocks uric acid.
  • Studies show that the lipogenic response to fructose is not a result of the metabolism of the fructose molecule itself, but rather from the general stimulation of lipogenesis and blocking of fatty acid oxidation.

Conclusions

  • Clinically, the intake of sugar-sweetened beverages is strongly linked with NAFLD, and reducing sugar or HFCS intake may have major benefits for patients with NAFLD.
  • Clinical studies to investigate the potential benefit of lowering uric acid are lacking and should be performed.
  • While there are many causes of NAFLD, the intake of fructose-containing sugars is likely to play a major role.

Points to Consider

  • Large and robust clinical trials in this area lacking. Most of the trials included were likely too short in duration to note fructose intake as a risk factor for NAFLD, especially since the development of a fatty liver takes months in animals.
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