This intra-hepatic lipid will promote the production and secretion of very low-density lipoprotein 1 (VLDL1) leading to an increase in post-prandial triglycerides. A vicious cycle occurs effecting insulin resistance as well. The lipid in the liver will increase insulin resistance resulting in increases in circulating diacylglycerol. Additionally, the insulin resistance will lead to further lipid deposit in the liver with sugar having a greater propensity to turn to fat (3). A downstream effect of increased apoCIII and apoB will lead to muscle lipid accumulation, and end in whole body insulin resistance. All of this metabolic dysregulation results from the direct route fructose initially takes to the liver.

Thanks for the link. If proven this would definitely be a bad outcome, but it doesn’t mean that a calorie deficit becomes a calorie surplus depending on the nutrient. If one is burning more than they’re consuming, the above is irrelevant insofar as weight gain is concerned. It’s relevant either way for diabetes.