MLXIPL and metabolic syndrome: Saturated enteral barriers let absorbed fructose flood the portal system, leading to increased activation of carbohydrate-responsive element-binding protein (ChREBP) and sterol regulatory element binding protein 1c (SREBP1c), stimulating ceramide synthesis, de novo lipogenesis (DNL), IR, fatty liver, and/or dyslipidemia [32,33,69].