Obesity is prevalent in Korea. An increase in food intake and a decrease in energy expenditure are responsible for obesity. Gut hormones play a role in controlling food intake. Obesity is suggested to be linked to common gastrointestinal functional disorders. Obesity is associated with an increased risk of gastroesophageal reflux disease, Barrett esophagus and esophageal adenocarcinoma. Epidemiologic studies indicate that obesity is associated with chronic gastrointestinal symptoms. This association suggests the possibility that obesity and functional gastrointestinal disorders may be pathophysiologically linked. However, data on the relationship between obesity and functional gastrointestinal disorders are inconsistent. In this paper, we review the role of gastrointestinal hormones in food intake and the relationship between obesity and functional gastrointestinal disorders.
Barrett Esophagus/*etiology ; Energy Intake ; Energy Metabolism ; Esophageal Neoplasms/*etiology ; Gastroesophageal Reflux/*etiology ; Humans ; Obesity/*complications/pathology ; Peptide Hormones/metabolism/physiology

BACKGROUND/AIMS: Barrett's esophagus is a premalignant lesion of the esophagus in which normal squamous epithelium is replaced by intestinalized columnar epithelium. In Korea, adenocarcinoma associated with Barrett's esophagus is rare compared with that of Western country. The purpose of this study was to investigate the immunohistochemical expression of p53 and Ki-67 in Barrett's esophagus which had predictive value for cancer risk in Korea. METHODS: Ninety five patients (43 male and 52 female, median age 44, range 21-75) who have been suspected to have Barrett's esophagus by endoscopic assessment were enrolled in this study. Alcian blue (pH 2.5) and high ion diamine stain for the evaluation of specialized intestinal metaplasia (SIM) and immunohistochemical stain for p53 and Ki-67 were done. RESULTS: 57.9% (55/95) of biopsies from the columnar lined esophagus showed SIM, but no dyspalsia. 56.4% (31/55) of Barrett's esophagus showed sulfomucin positive colonic metaplasia. The p53 expression was observed in 10.9% (6/55) of the patients of Barrett's esophagus and all of them showed colonic metaplasia. Ki-67 labeling index showed no difference significantly. CONCLUSIONS: In Korea, 10.9% of Barrett's esophagus had p53 mutation and moreover all of them had colonic metaplasia. Consequently, we expect that these patients have high risk of developing dysplasia and adenocarcinoma and need careful follow-up.
Adenocarcinoma/etiology/genetics ; Adult ; Aged ; Barrett Esophagus/complications/*metabolism ; Esophageal Neoplasms/etiology/genetics ; Female ; Humans ; Immunohistochemistry ; Ki-67 Antigen/*metabolism ; Male ; Middle Aged ; Risk Factors ; Tumor Suppressor Protein p53/*metabolism

Adenocarcinoma ; etiology ; metabolism ; pathology ; Barrett Esophagus ; complications ; epidemiology ; etiology ; metabolism ; pathology ; Biomarkers, Tumor ; metabolism ; Biopsy ; CDX2 Transcription Factor ; Esophagogastric Junction ; pathology ; Esophagus ; pathology ; Homeodomain Proteins ; metabolism ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Keratin-20 ; metabolism ; Keratin-7 ; metabolism ; Mucous Membrane ; pathology ; Precancerous Conditions ; metabolism ; pathology

PURPOSE: It is known that cyclooxygenase (COX)-2 expression is increased in Barrett's esophagus and esophageal adenocarcinomas. We studied COX-2 expression and the effect sulindac has on the genesis of Barrett's esophagus and adenocarcinoma in rats undergoing esophagogastroduodenal anastomosis (EGDA). MATERIALS AND METHODS: Fifty-one rats were divided into a control group (n=27), a 500ppm sulindac-treated group (n=15) and 1000 ppm sulindac-treated group (n=9). Randomly selected rats were killed by diethyl ether inhalation at 20 and 40 weeks after surgery. RESULTS: At 40 weeks, rats treated with 1000 ppm sulindac showed narrower esophageal diameter and milder inflammation than the control rats. At 40 weeks, the incidence of Barrett's esophagus was similar between control and sulindac-treated groups, but the incidence of adenocarcinoma was significantly lower in the 1000ppm sulindac-treated group than either the control or 500 ppm sulindac-treated groups. COX-2 was significantly increased in the lower esophagus of control rats killed at 40 weeks. Cyclin D1 expression was negligible in the sulindac- treated group compared with the control group. CONCLUSION: We suggest that the chemopreventive effect of sulindac is related to decreased COX-2 and cyclin D1 expression, which may be influenced by reduced inflammation.
Adenocarcinoma/etiology/metabolism/*prevention & control ; Animals ; Antineoplastic Agents/therapeutic use ; Barrett Esophagus/etiology/metabolism/prevention & control ; Blotting, Western ; Cyclin D1/metabolism ; Cyclooxygenase 2/metabolism ; Duodenogastric Reflux/*complications ; Esophageal Neoplasms/etiology/metabolism/*prevention & control ; Immunohistochemistry ; Male ; Proliferating Cell Nuclear Antigen/metabolism ; Rats ; Rats, Sprague-Dawley ; Sulindac/*therapeutic use