PMID- 26671515 OWN - NLM STAT- MEDLINE DCOM- 20161024 LR - 20240324 IS - 1473-5687 (Electronic) IS - 0954-691X (Print) IS - 0954-691X (Linking) VI - 28 IP - 3 DP - 2016 Mar TI - Role of body composition and metabolic profile in Barrett's oesophagus and progression to cancer. PG - 251-60 LID - 10.1097/MEG.0000000000000536 [doi] AB - BACKGROUND AND AIMS: The aim of this study was to evaluate the risk for Barrett's oesophagus (BE) on the basis of body composition, metabolic pathways, adipokines and metabolic syndrome (MS), as well as their role in cancer progression. METHODS: In patients with and without BE at gastroscopy, data on MS, BMI, waist/hip ratio for abdominal obesity (AO) and body fat percentage by bioimpedance were obtained. Fasting plasma glucose, insulin, HbA1c, lipid, serum adiponectin and leptin levels were measured. The homoeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. Histological findings for BE were correlated with the above parameters. Risk factors for BE identified using univariate analysis were entered into a multivariate logistic regression analysis. RESULTS: A total of 250 patients and 224 controls (F/M: 189/285, mean age 58.08+/-15.51 years) were enroled. In the BE and control groups, 39.6 versus 31.3% were overweight, 32 versus 22.8% were obese, 75.6 versus 51.3% had AO, and 28.1 versus 18.9% were metabolically obese, respectively. AO [odds ratio (OR) 3.08], increased body fat percentage (OR 2.29), and higher BMI (overweight: OR 2.04; obese: OR 2.26) were significantly associated with BE. A positive trend was found in Normal Weight Obese Syndrome (OR 1.69). MS was associated with BE (overweight: OR 3.05; obese: OR 5.2; AO: OR 8.08). Insulin levels (P=0.05) and HOMA-IR (P<0.001) were higher in BE. AO was the only independent risk factor associated with BE (OR 1.65; P=0.02) and high-grade dysplasia (OR 2.44) on multivariate analysis. CONCLUSION: AO was strongly associated with BE and dysplasia. BE was associated with MS and higher insulin/HOMA-IR, suggesting the activation of specific metabolic pathways in patients with altered body composition. FAU - Di Caro, Simona AU - Di Caro S AD - Departments of aGastroenterology bMedicine, Centre for Obesity Research, University College London Hospital, London, UK cDepartment of Gastroenterology, Busto Arstizio Hospital, Milan dDepartment of Neuroscience, Tor Vergata University, Rome, Italy. FAU - Cheung, Wui Hang AU - Cheung WH FAU - Fini, Lucia AU - Fini L FAU - Keane, Margaret G AU - Keane MG FAU - Theis, Belinda AU - Theis B FAU - Haidry, Rehan AU - Haidry R FAU - Di Renzo, Laura AU - Di Renzo L FAU - De Lorenzo, Antonino AU - De Lorenzo A FAU - Lovat, Laurence AU - Lovat L FAU - Batterham, Rachel L AU - Batterham RL FAU - Banks, Matthew AU - Banks M LA - eng GR - RP-2015-06-005/DH_/Department of Health/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Eur J Gastroenterol Hepatol JT - European journal of gastroenterology & hepatology JID - 9000874 RN - 0 (Adipokines) RN - 0 (Biomarkers) RN - 0 (Blood Glucose) RN - 0 (Glycated Hemoglobin A) RN - 0 (Insulin) RN - 0 (Lipids) RN - 0 (hemoglobin A1c protein, human) RN - Adenocarcinoma Of Esophagus SB - IM MH - Adenocarcinoma/*epidemiology/pathology MH - Adipokines/blood MH - *Adiposity MH - Adult MH - Aged MH - Barrett Esophagus/*epidemiology/pathology MH - Biomarkers/blood MH - Blood Glucose/analysis MH - Body Mass Index MH - Case-Control Studies MH - Chi-Square Distribution MH - Disease Progression MH - Esophageal Neoplasms/*epidemiology/pathology MH - Female MH - Gastroscopy MH - Glycated Hemoglobin/analysis MH - Humans MH - Insulin/blood MH - Lipids/blood MH - Logistic Models MH - London/epidemiology MH - Male MH - Metabolic Syndrome/*blood/diagnosis/epidemiology MH - Middle Aged MH - Multivariate Analysis MH - Obesity, Abdominal/diagnosis/epidemiology/*physiopathology MH - Odds Ratio MH - Precancerous Conditions/*epidemiology/pathology MH - Prevalence MH - Prospective Studies MH - Risk Assessment MH - Risk Factors MH - Waist-Hip Ratio PMC - PMC4739314 EDAT- 2015/12/17 06:00 MHDA- 2016/10/25 06:00 PMCR- 2016/02/03 CRDT- 2015/12/17 06:00 PHST- 2015/12/17 06:00 [entrez] PHST- 2015/12/17 06:00 [pubmed] PHST- 2016/10/25 06:00 [medline] PHST- 2016/02/03 00:00 [pmc-release] AID - 10.1097/MEG.0000000000000536 [doi] PST - ppublish SO - Eur J Gastroenterol Hepatol. 2016 Mar;28(3):251-60. doi: 10.1097/MEG.0000000000000536.