Publication Name	World Journal of Gastroenterology
Manuscript ID	6631
Country	Japan

Received	2013-10-31 17:08
Peer-Review Started	2013-11-14 22:22
To Make the First Decision	2014-01-09 12:38
Return for Revision	2014-03-06 12:12
Revised	2014-03-18 16:43
Second Decision	2014-06-13 15:54
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2014-06-13 16:22
Articles in Press	2014-06-13 16:24
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2014-10-15 20:37
Publish the Manuscript Online	2014-10-29 19:34

ISSN	1007-9327 (print) and 2219-2840 (online)
Open Access
Copyright
Article Reprints	For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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Publisher	Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website	http://www.wjgnet.com

Category	Gastroenterology & Hepatology
Manuscript Type	Topic Highlights
Article Title	Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver
Manuscript Source	Invited Manuscript
All Author List	Jinyao Liu
Funding Agency and Grant Number
Corresponding Author	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
Key Words	Alcohol; Fatty liver; Tumor necrosis factor-a; Hepatic stellate cell; Bone marrow-derived cell; Alcoholic liver disease
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-? 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)-? 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-a overproduction in ethanol-induced hepatosteatosis. Carvedilol may attenuate the progression of ethanol-induced hepatosteatosis by suppressing sympathetic activity.
Publish Date	2014-10-29 19:34
Citation	Liu J. Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver. World J Gastroenterol 2014; 20(40): 14672-14685
URL	http://www.wjgnet.com/1007-9327/full/v20/i40/14672.htm
DOI	http://dx.doi.org/10.3748/wjg.v20.i40.14672

Full Article (PDF)	WJG-20-14672.pdf
Full Article (Word)	WJG-20-14672.doc
Manuscript File	6631-Review.docx
Answering Reviewers	6631-Answering reviewers.pdf
Copyright License Agreement	6631-Copyright assignment.pdf
Non-Native Speakers of English Editing Certificate	6631-Language certificate.pdf
Peer-review Report	6631-Peer review(s).pdf
Scientific Misconduct Check	6631-CrossCheck.jpg
Scientific Editor Work List	6631-Scientific editor work list.pdf