Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver

Core Tip

Core tip: Alcohol induces fatty liver by increasing the nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide ratio; increasing the activity of sterol regulatory element-binding protein (SREBP)-1, plasminogen activator inhibitor (PAI)-1, and early growth response-1; and decreasing peroxisome proliferator-activated receptor-α activity in liver. Alcohol activates the innate immune system and induces an imbalance in the immune response followed by the activation of Kupffer cell-derived tumor necrosis factor (TNF)-α overproduction, which is responsible for the dysregulated SREBP-1 and PAI-1 activity. Bone marrow-derived cells and sympathetic hyperactivity-activated hepatic stellate cells are also responsible for TNF-α overproduction in ethanol-induced hepatosteatosis. Carvedilol may attenuate the progression of ethanol-induced hepatosteatosis by suppressing sympathetic activity.