[King Grub]

In summary, there has been a marked rise in sugar and HFCS intake that has paralleled the rise of NAFLD. Experimentally the fructose component of sugar and HFCS appears to have a major role in inducing fatty liver by both stimulating de novo lipogenesis and blocking β-fatty acid oxidation. Evidence suggests these effects are due to the unique metabolism of fructose by fructokinase that leads to a fall in ATP with nucleotide turnover and uric acid generation. The prooxidative and proinflammatory effects of uric acid lead to increases in gut permeability and endotoxemia that exacerbates the lipogenic process in the liver, and coupled with mitochondrial dysfunction results in NAFLD. Clinically the intake of sugary sweetened beverages is strongly linked with NAFLD. Reducing sugar or HFCS intake may have a major benefit on NAFLD. Clinical studies to investigate the potential benefit of lowering uric acid should also be performed. While there are many causes of NAFLD, the intake of fructose containing sugars is likely to have a major role.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5893377/