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Summary

Background

The role of excess fructose intake in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) has recently received increasing attention, but the pathophysiology of this relationship has been only partly elucidated.

Aim

To provide an overview of the potential role played by fructose in the pathogenesis of NAFLD by focusing on both indirect and direct harmful effects.

Methods

Experimental and clinical studies which investigated the relation of fructose with NAFLD are reviewed.

Results

Several factors may potentially contribute to fructose-induced NAFLD, including the induction of the metabolic syndrome, copper deficiency, bacterial translocation from the gut to the liver, the formation of advanced glycation endproducts and a direct dysmetabolic effect on liver enzymes.

Conclusions

Experimentally-increased fructose intake recapitulates many of the pathophysiological characteristics of the metabolic syndrome in humans, which may in turn lead to NAFLD. However, the majority of experimental studies tend to involve feeding excessively high levels of fructose (60–70% of total energy intake) which is not reflective of average human intake. Hopefully, the combination of in vivo, in vitro and genetic research will provide substantial mechanistic evidence into the role of fructose in NAFLD development and its complications.