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©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 14, 2015; 21(6): 1784-1793
Published online Feb 14, 2015. doi: 10.3748/wjg.v21.i6.1784
Published online Feb 14, 2015. doi: 10.3748/wjg.v21.i6.1784
In vitro identification of nonalcoholic fatty liver disease-related protein hnRNPM
Jun-ichi Takino, Kentaro Nagamine, Takamitsu Hori, Department of Biochemistry, Faculty of Pharmaceutical Sciences, Hiroshima International University, Hiroshima 737-0112, Japan
Masayoshi Takeuchi, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, Ishikawa 920-0293, Japan
Author contributions: Takeuchi M designed the study and contributed experimental reagents; Takino J and Nagamine K performed the study; Nagamine K analyzed data; Takino J wrote the paper; and Hori T reviewed the paper.
Supported by Grants from the Japan Society for the Promotion of Science, No. 22300264 and No. 25282029.
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: Masayoshi Takeuchi, PhD, Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada-machi, Kahoku, Ishikawa 920-0293, Japan. takeuchi@kanazawa-med.ac.jp
Telephone: +81-76-2862211 Fax: +81-76-2863652
Received: July 18, 2014
Peer-review started: July 20, 2014
First decision: August 15, 2014
Revised: August 29, 2014
Accepted: October 14, 2014
Article in press: October 15, 2014
Published online: February 14, 2015
Peer-review started: July 20, 2014
First decision: August 15, 2014
Revised: August 29, 2014
Accepted: October 14, 2014
Article in press: October 15, 2014
Published online: February 14, 2015
Core Tip
Core tip: Excessive intake of fructose contributes to the development of nonalcoholic fatty liver disease and to the progression of the disease to nonalcoholic steatohepatitis. Fructose is metabolized to glyceraldehyde, which is a precursor of glyceraldehyde-derived advanced glycation end-products (Glycer-AGEs). We showed that intracellular Glycer-AGEs were formed in the presence of high concentrations of fructose. Additionally, heterogeneous nuclear ribonucleoprotein M (hnRNPM) was identified as one of the target proteins for glycation. These results suggest that the glyceraldehyde-modified hnRNPM resulting from the exposure of the cells to high concentrations of fructose, alters gene expression and causes adverse effects in hepatocytes.