Association Between Visceral Fat and Inflammatory Cytokines in Reflux Esophagitis

Article: The Effect of abdominal visceral fat, circulating inflammatory cytokines, and leptin levels on reflux esophagitis CC This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons. org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The results of several previous studies have suggested that abdominal obesity is an important risk factor for reflux eso-phagitis. 1,2 Among factors related to obesity, visceral fat is more associated with erosive esophagitis than body mass index (BMI). 3 Physiologic abnormalities related to prolonged esoph-ageal acid exposure have been found to occur more frequently in obese individuals than in those with normal weight. Obese subjects revealed abnormal esophageal manometric findings such as nonspecific motility disorder, nutcracker esophagus, and hypo-tensive lower esophageal sphincter as the most common mano-metric results. 4 Transient relaxations of the lower esophageal sphincter (TRLES) is also reported to be more common in patients with obesity. The main stimulus for TRLES is gastric dis-tension especially in the gastric fundus. 5 Pandofino et al 6 reported esophageal manometric findings suggesting that the pressure morphology within and across the esophagogastric junction were altered in obesity, which could augment the flow of gastric juices into the esophageal lumen. This anatomical disruption of the esophagogastric junction results in further hiatal hernia formation. Esophageal mucosal injury is associated with increased exposure to gastric acid. However, maintenance of chronic esoph-ageal mucosal inflammation and esophageal metaplasia such as Barrett's esophagus (BE) or esophageal carcinoma in obese subjects have been proposed to increase inflammatory cytokines from visceral adipose tissue. 7 The relationship between obesity and esophageal neoplasia may be due to alterations in the secretion of adipokines such as adiponection and leptin. Adiponection has an anti-inflammatory effect and stimulates apoptosis, which shows inverse relationship between obesity and adiponection. 8 Leptin, a satiety hormone, is secreted by adipocytes and gastric chief cells. Esophageal epithelial cells express leptin receptors. In an esoph-ageal adenocarcinoma cell line, leptin has been shown to stimulate cell proliferation and inhibit apoptosis via cyclooxygenase-2 acti