MLXIPL and Hepatic steatosis: Exponential fructose consumption is also recognized as an important driving force for the development of NAFLD, since fructose overconsumption in mice and humans triggers lipogenesis by activating the transcription factors SREBP1c and ChREBP and augmenting the expression of lipogenic enzymes, influencing hepatic steatosis, IR, dyslipoproteinemia, and adiposity (16–26).