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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 14, 2014; 20(34): 12161-12170
Published online Sep 14, 2014. doi: 10.3748/wjg.v20.i34.12161
Published online Sep 14, 2014. doi: 10.3748/wjg.v20.i34.12161
TLR4 signaling and the inhibition of liver hepcidin expression by alcohol
Emily Zmijewski, Sizhao Lu, Duygu Dee Harrison-Findik, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5820, United States
Author contributions: Lu S and Zmijewski E performed the experiments and helped with the manuscript; Harrison-Findik DD designed the study, and wrote and edited the manuscript.
Supported by NIH grant No. R01AA017738 (to Harrison-Findik DD); and University of Nebraska Medical Center Undergraduate Scholarship (to Lu S)
Correspondence to: Duygu Dee Harrison-Findik, PhD, Department of Internal Medicine, University of Nebraska Medical Center, 95820 UNMC, DRC I, Omaha, NE 68198-5820, United States. dharrisonfindik@unmc.edu
Telephone: +1-402-5596355 Fax: +1-402-5596494
Received: February 12, 2014
Revised: April 12, 2014
Accepted: May 19, 2014
Published online: September 14, 2014
Revised: April 12, 2014
Accepted: May 19, 2014
Published online: September 14, 2014
Core Tip
Core tip: Chronic alcohol intake induces inflammation and also alters iron homeostasis by inhibiting the expression of hepcidin in the liver. Besides being the key iron-regulatory hormone, hepcidin also acts as an acute phase protein, and is induced by endotoxin and inflammation. The mechanisms by which chronic alcohol consumption can lead to the suppression of hepcidin expression despite the presence of inflammatory processes in the liver are unknown. This study investigates these mechanisms by using wildtype and toll-like receptor 4 mutant mice, and chronic alcohol administration as a model.