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World J Gastrointest Pathophysiol. Nov 15, 2014; 5(4): 534-549
Published online Nov 15, 2014. doi: 10.4291/wjgp.v5.i4.534
Published online Nov 15, 2014. doi: 10.4291/wjgp.v5.i4.534
Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma
Leo Alexandre, Elizabeth Long, Ian LP Beales, Norwich Medical School, University of East Anglia, Norwich, Norfolk NR4 7TJ, United Kingdom
Leo Alexandre, Ian LP Beales, Department of Gastroenterology, Norfolk and Norwich University Hospital, Norwich, Norfolk NR4 7UY, United Kingdom
Author contributions: Beales ILP conceived of the original idea by discussion with Alexandre L and Long E; Alexandre L, Long E and Beales ILP individually researched and wrote initial drafts of separate parts of the manuscript; Beales ILP co-ordinated the research and writing and wrote the final draft of the manuscript and is the guarantor of the paper.
Correspondence to: 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
Telephone: +44-1603-591003 Fax: +44-1603-593752
Received: May 6, 2014
Revised: August 7, 2014
Accepted: September 4, 2014
Published online: November 15, 2014
Processing time: 197 Days and 7.6 Hours
Revised: August 7, 2014
Accepted: September 4, 2014
Published online: November 15, 2014
Processing time: 197 Days and 7.6 Hours
Core Tip
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.