BPG is committed to discovery and dissemination of knowledge
Articles Published Processes
11/19/2014 10:25:00 AM | Browse: 1082 | Download: 1280
Publication Name World Journal of Gastrointestinal Pathophysiology
Manuscript ID 11128
Country United Kingdom
Received
2014-05-06 08:52
Peer-Review Started
2014-05-06 19:47
To Make the First Decision
2014-07-10 17:25
Return for Revision
2014-07-11 14:18
Revised
2014-08-07 15:04
Second Decision
2014-09-10 09:04
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-09-10 09:26
Articles in Press
2014-09-10 09:26
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
2014-10-31 10:36
Publish the Manuscript Online
2014-11-19 10:25
ISSN 2150-5330 (online)
Open Access
Copyright
Article Reprints For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
Permissions For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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 Review
Article Title Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma
Manuscript Source Unsolicited Manuscript
All Author List Leo Alexandre, Elizabeth Long and Ian LP Beales
Funding Agency and Grant Number
Corresponding Author Dr. Ian LP Beales, MD, FRCP, Clinical Senior Lecturer and Honorary Consultant Gastroenterologist, Department of Gastroenterology, Norfolk and Norwich University Hospital, Colney Lane, Norwich, Norfolk NR4 7TJ, United Kingdom. i.beales@uea.ac.uk
Key Words Adipose; Body mass index; Reflux; Barrett’s esophagus
Core Tip Excess adipose tissue, particularly visceral obesity, is an important risk factor for esophageal adenocarcinoma (EAC). The mechanisms involve both the promotion of gastro-esophageal reflux and reflux-independent mechanisms. Abnormal secretion of the adipokines leptin and adiponectin from adipose tissue in obesity may promote the development of EAC. Increased leptin levels are an independent risk factor for EAC and leptin enhances proliferation and invasion and inhibits apoptosis in Barrett’s cell lines. Relative adiponectin deficiency is an independent risk factor for EAC and adiponectin blocks the cancer promoting effects of leptin in experimental models. Obesity may influence EAC development via adipokine secretion.
Publish Date 2014-11-19 10:25
Citation Alexandre L, Long E, Beales ILP. Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma. World J Gastrointest Pathophysiol 2014; 5(4): 534-549
URL http://www.wjgnet.com/2150-5330/full/v5/i4/534.htm
DOI http://dx.doi.org/10.4291/wjgp.v5.i4.534
Full Article (PDF) WJGP-5-534.pdf
Full Article (Word) WJGP-5-534.doc
Manuscript File 11128-Review.docx
Answering Reviewers 11128-Answering reviewers.pdf
Copyright License Agreement 11128-Copyright assignment.pdf
Peer-review Report 11128-Peer review(s).pdf
Scientific Misconduct Check 11128-CrossCheck.jpg
Scientific Editor Work List 11128-Scientific editor work list.pdf