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World J Gastroenterol. Oct 28, 2014; 20(40): 14672-14685
Published online Oct 28, 2014. doi: 10.3748/wjg.v20.i40.14672
Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver
Jinyao Liu
Jinyao Liu, Department of Legal Medicine, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan
Author contributions: Liu J was the sole contributor to this manuscript.
Correspondence to: Jinyao Liu, MD, PhD, Department of Legal Medicine, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan. czhliu@yamaguchi-u.ac.jp
Telephone: +81-836-222234 Fax: +81-836-222232
Received: October 25, 2013
Revised: March 18, 2014
Accepted: June 13, 2014
Published online: October 28, 2014
Processing time: 369 Days and 7.2 Hours
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.