Fructose contributes to NAFLD by providing a substrate for increased FA synthesis and activating hepatic de novo lipogenesis, which it promotes directly by upregulating SREBP1c [31], and indirectly by uric acid production, which reduces mitochondrial β-oxidation resulting in oxidative stress, hepatic IR, and endoplasmic reticulum (ER) stress [32, 33]. Here, SREBF1 is linked to metabolic dysfunction-associated steatotic liver disease.