Alcohol contributes to fatty liver through various mechanisms. Alcohol increases the NADH/NAD+ ratio, which inhibits fatty acid oxidation and tricarboxylic acid cycle reactions, leading to fat accumulation in the liver (Purohit 2009; You 2004). Alcohol also increases the activity of sterol regulatory element-binding protein-1 (SREBP-1), plasminogen activator inhibitor-1 (PAI-1), and early growth response-1, while decreasing peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activity, which promotes lipogenesis and inhibits fat oxidation (Liu 2014; You 2004). Alcohol also activates the innate immune system, leading to Kupffer cell-derived tumor necrosis factor-alpha (TNF-alpha) overproduction, which upregulates SREBP-1 and PAI-1 activity (Liu 2014). Chronic alcohol consumption also retards lipophagy, which exacerbates steatosis (Yang 2019). The papers suggest that PPAR-alpha agonists, adiponectin, interleukin-6, and carvedilol may attenuate alcoholic fatty liver by upregulating PPAR-alpha and insulin signaling pathways while downregulating SREBP-1 activity and suppressing TNF-alpha production (Purohit 2009; You 2004; Liu 2014).
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