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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 8, 2016; 8(4): 211-225
Published online Feb 8, 2016. doi: 10.4254/wjh.v8.i4.211
Published online Feb 8, 2016. doi: 10.4254/wjh.v8.i4.211
Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver
Sizhao Lu, Robert G Bennett, Department of Biochemistry, University of Nebraska Medical Center, Omaha, NE 68198-5870, United States
Robert G Bennett, Division of Endocrinology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-4130, United States
Robert G Bennett, Kusum K Kharbanda, Nebraska-Western Iowa VA Health Care System, Omaha, NE 68105, United States
Kusum K Kharbanda, Duygu Dee Harrison-Findik, Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-2000, United States
Author contributions: Lu S contributed to study design, data acquisition and drafting of the manuscript; Harrison-Findik DD obtained funding, contributed to study concept and supervision, and critical revision of the manuscript; Bennett RG and Kharbanda K helped with technical support and critical reading of the manuscript.
Supported by NIH grant No. R01AA017738 (to Harrison-Findik DD); and University of Nebraska Medical Center Graduate Assistantship/Fellowship (to Lu S).
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of University of Nebraska Medical Center (IACUC protocol No. 03-075-10-FC).
Conflict-of-interest statement: The authors declare no conflict of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Duygu Dee Harrison-Findik, DVM, PhD, Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Nebraska Medical Center, 92000 UNMC, Omaha, NE 68198-2000, United States. dufindik@gmail.com
Telephone: +1-402-5596209 Fax: +1-402-5599004
Received: August 2, 2015
Peer-review started: August 3, 2015
First decision: September 29, 2015
Revised: October 14, 2015
Accepted: November 13, 2015
Article in press: November 13, 2015
Published online: February 8, 2016
Processing time: 176 Days and 20.1 Hours
Peer-review started: August 3, 2015
First decision: September 29, 2015
Revised: October 14, 2015
Accepted: November 13, 2015
Article in press: November 13, 2015
Published online: February 8, 2016
Processing time: 176 Days and 20.1 Hours
Core Tip
Core tip: Due to obesity epidemic the incidence of non-alcoholic fatty liver disease (NAFLD) is on the rise. Iron contributes to disease severity and the expression of key iron regulatory hormone, hepcidin is modulated in NAFLD patients. The underlying mechanisms are unknown. We have generated hepcidin knockout mice with iron overload phenotype. This study investigates the role of hepcidin in NAFLD by using high fat and high sucrose-fed knockout mice as an experimental model of NAFLD. Our findings showed attenuated steatosis and early fibrosis development suggesting a role for hepcidin in the regulation of metabolic processes in the liver, and in NAFLD.