title: Role of Obesity in the Pathogenesis and Progression of Barrett's Esophagus.
abstract: Central obesity is involved in the pathogenesis and progression of Barrett's esophagus to esophageal adenocarcinoma. Involved are likely both mechanical and nonmechanical effects. Mechanical effects of increased abdominal fat cause disruption of the gastroesophageal reflux barrier leading to increased reflux events. Nonmechanical effects may be mediated by inflammation, via classically activated macrophages, pro-inflammatory cytokines, and adipokines such as Leptin, all of which likely potentiate reflux-mediated inflammation. Insulin resistance, associated with central obesity, is also associated with both Barrett's pathogenesis and progression to adenocarcinoma. Molecular pathways activated in obesity, inflammation and insulin resistance overlap with those involved in Barrett's pathogenesis and progression.
authors.affiliation: Division of Gastroenterology and Liver Diseases, Digestive Health Institute, University Hospitals Case Medical Center, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
authors.forename: Apoorva Krishna
authors.initials: AK
authors.lastname: Chandar
authors.affiliation: Barrett's Esophagus Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 1st Street South West, Rochester, MN 55905, USA. Electronic address: iyer.prasad@mayo.edu.
authors.forename: Prasad G
authors.initials: PG
authors.lastname: Iyer
mesh_terms: D052242:Adiponectin / Q000097:blood; D001471:Barrett Esophagus / Q000097:blood / Q000209:etiology*; D005764:Gastroesophageal Reflux / Q000150:complications; D006551:Hernia, Hiatal / Q000150:complications; D006801:Humans; D007249:Inflammation / Q000150:complications; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D056128:Obesity, Abdominal / Q000150:complications* / Q000378:metabolism / Q000628:therapy
chemical_list: D052242:Adiponectin; D007328:Insulin; D020738:Leptin
keywords: Adiponectin; Barrett’s esophagus; Esophageal adenocarcinoma; Gastroesophageal reflux disease; Inflammation; Insulin resistance; Leptin; Obesity