Apoorva Krishna Chandar1, Swapna Devanna2, Chang Lu3, Siddharth Singh2, Katarina Greer1, Amitabh Chak1, Prasad G Iyer4. 1. Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland; Digestive Health Institute, University Hospitals Case Medical Center, Cleveland, Ohio. 2. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. 3. Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland. 4. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Electronic address: iyer.prasad@mayo.edu.
Abstract
BACKGROUND & AIMS: Metabolically active visceral fat may be associated with esophageal inflammation, metaplasia, and neoplasia. We performed a meta-analysis to evaluate the association of serum adipokines and insulin with Barrett's esophagus (BE). METHODS: We performed a systematic search of multiple electronic databases, through April 2015, to identify all studies reporting associations between leptin, adiponectin, insulin, insulin resistance, and risk of BE in adults. Comparing the highest study-specific category with the reference category for each hormone, we estimated the summary adjusted odds ratio (aOR) and 95% confidence intervals (CI), using a random effects model. RESULTS: We identified 9 observational studies (10 independent cohorts; 1432 patients with BE total, and 3550 control subjects). Meta-analysis revealed that high serum level of leptin was associated with 2-fold higher risk of BE (BE cases vs population control subjects in 5 studies: aOR, 2.23; 95% CI, 1.31-3.78; I(2), 59%). Total serum level of adiponectin was not associated with BE (BE cases vs population control subjects in 5 studies: aOR, 0.79; 95% CI, 0.46-1.34; I(2), 65%), although 1 study observed decreased risk of BE with increased level of low-molecular-weight adiponectin. High serum level of insulin was associated with increased risk of BE (BE cases vs population control subjects in 3 studies: aOR, 1.74; 95% CI, 1.14-2.65; I(2), 0), whereas insulin resistance was not associated with increased risk of BE (BE cases vs gastroesophageal reflux disease control subjects in 2 studies: aOR, 0.98; 95% CI, 0.42-2.30; I(2), 64%). CONCLUSIONS: Increased serum levels of leptin and insulin are associated with increased risk of BE, compared with population control subjects. In contrast, increased total serum levels of adiponectin and insulin do not seem to modify BE risk. Well-designed longitudinal studies of incident BE are needed to clarify existing associations of serum adipokines and insulin with BE.
BACKGROUND & AIMS: Metabolically active visceral fat may be associated with esophageal inflammation, metaplasia, and neoplasia. We performed a meta-analysis to evaluate the association of serum adipokines and insulin with Barrett's esophagus (BE). METHODS: We performed a systematic search of multiple electronic databases, through April 2015, to identify all studies reporting associations between leptin, adiponectin, insulin, insulin resistance, and risk of BE in adults. Comparing the highest study-specific category with the reference category for each hormone, we estimated the summary adjusted odds ratio (aOR) and 95% confidence intervals (CI), using a random effects model. RESULTS: We identified 9 observational studies (10 independent cohorts; 1432 patients with BE total, and 3550 control subjects). Meta-analysis revealed that high serum level of leptin was associated with 2-fold higher risk of BE (BE cases vs population control subjects in 5 studies: aOR, 2.23; 95% CI, 1.31-3.78; I(2), 59%). Total serum level of adiponectin was not associated with BE (BE cases vs population control subjects in 5 studies: aOR, 0.79; 95% CI, 0.46-1.34; I(2), 65%), although 1 study observed decreased risk of BE with increased level of low-molecular-weight adiponectin. High serum level of insulin was associated with increased risk of BE (BE cases vs population control subjects in 3 studies: aOR, 1.74; 95% CI, 1.14-2.65; I(2), 0), whereas insulin resistance was not associated with increased risk of BE (BE cases vs gastroesophageal reflux disease control subjects in 2 studies: aOR, 0.98; 95% CI, 0.42-2.30; I(2), 64%). CONCLUSIONS: Increased serum levels of leptin and insulin are associated with increased risk of BE, compared with population control subjects. In contrast, increased total serum levels of adiponectin and insulin do not seem to modify BE risk. Well-designed longitudinal studies of incident BE are needed to clarify existing associations of serum adipokines and insulin with BE.
Authors: Josef V Silha; Michal Krsek; Jan V Skrha; Petr Sucharda; B L G Nyomba; Liam J Murphy Journal: Eur J Endocrinol Date: 2003-10 Impact factor: 6.664
Authors: Anna M Wolf; Dominik Wolf; Holger Rumpold; Barbara Enrich; Herbert Tilg Journal: Biochem Biophys Res Commun Date: 2004-10-15 Impact factor: 3.575
Authors: Bradley J Kendall; Joel H Rubenstein; Michael B Cook; Thomas L Vaughan; Lesley A Anderson; Liam J Murray; Nicholas J Shaheen; Douglas A Corley; Apoorva K Chandar; Li Li; Katarina B Greer; Amitabh Chak; Hashem B El-Serag; David C Whiteman; Aaron P Thrift Journal: Clin Gastroenterol Hepatol Date: 2016-06-02 Impact factor: 11.382