Publication Name	World Journal of Biological Chemistry
Manuscript ID	12261
Country	South Korea

Received	2014-06-29 13:56
Peer-Review Started	2014-06-29 19:02
To Make the First Decision	2014-09-16 10:51
Return for Revision	2014-09-18 09:20
Revised	2014-10-29 12:34
Second Decision	2014-11-28 14:57
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2014-12-10 17:25
Articles in Press	2014-12-10 17:25
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2015-01-30 13:27
Publish the Manuscript Online	2015-02-05 14:08

ISSN	1949-8454 (online)
Open Access	This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/ licenses/by-nc/4.0/
Copyright	© The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
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Category	Endocrinology & Metabolism
Manuscript Type	Review
Article Title	Chronic alcohol consumption potentiates the developmentof diabetes through pancreatic b-cell dysfunction
Manuscript Source	Invited Manuscript
All Author List	Ji Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Jae Woo Kim and Won-Ho Kim
Funding Agency and Grant Number	Funding Agency Grant Number Korean National Institute of Health 4845-302-201-13
Corresponding Author	Won-Ho Kim, PhD, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, #187 Osong Saengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea. jhkwh@nih.go.kr
Key Words	Ethanol consumption; Type 2 diabetes; Pancreatic β-cells; Glucokinase; Metabolic syndrome
Core Tip	Chronic ethanol consumption induces Glucokinase (GCK) downregulation and inactivation through Tyr nitration, resulting in pancreatic β-cell apoptosis and dysfunction. Additionally, GCK proteins nitrated following ethanol treatment may be more susceptible to ubiquitination and consequent degradation than are native proteins of control cells. Peroxynitritemediated GCK downregulation or inactivation may perturb glucose metabolism and cellular antioxidant defense mechanisms, increasing susceptibility to insulin resistance and type-2 diabetes. Furthermore, peroxynitrite-generated activating transcription factor 3 may play as a major upstream regulator of GCK downregulation in β-cell dysfunction and apoptosis.
Publish Date	2015-02-05 14:08
Citation	Kim JY, Lee DY, Lee YJ, Park KJ, Kim KH, Kim JW, Kim WH. Chronic alcohol consumption potentiates the development of diabetes through pancreatic β-cell dysfunction. World J Biol Chem 2015; 6(1): 1-15
URL	http://www.wjgnet.com/1949-8454/full/v6/i1/1.htm
DOI	http://dx.doi.org/10.4331/wjbc.v6.i1.1

Full Article (PDF)	WJBC-6-1.pdf
Full Article (Word)	WJBC-6-1.doc
Manuscript File	12261-Review.docx
Answering Reviewers	12261-Answering reviewers.pdf
Conflict-of-Interest Disclosure Form	12261-Conflict-of-interest statement.pdf
Copyright License Agreement	12261-Copyright assignment.pdf
Peer-review Report	12261-Peer review(s).pdf
Scientific Misconduct Check	12261-CrossCheck.jpg
Scientific Editor Work List	12261-Scientific editor work list.pdf