Copyright
©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 21, 2014; 20(23): 7381-7391
Published online Jun 21, 2014. doi: 10.3748/wjg.v20.i23.7381
Published online Jun 21, 2014. doi: 10.3748/wjg.v20.i23.7381
Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease
Kouichi Miura, Hirohide Ohnishi, Department of Gastroenterology, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Author contributions: Miura K and Ohnishi H contributed to the acquisition of data and wrote this article.
Supported by JSPS [Grant-in-Aid for Scientific Research (C)] (to Miura K)
Correspondence to: Kouichi Miura, MD, PhD, Department of Gastroenterology, Akita University Graduate School of Medicine, 1-1-1 Hondo Akita-shi, Akita 010-8543, Japan. miura116@doc.med.akita-u.ac.jp
Telephone: +81-18-8846104 Fax: +81-18-8362611
Received: November 27, 2013
Revised: January 7, 2014
Accepted: January 20, 2014
Published online: June 21, 2014
Processing time: 205 Days and 19.3 Hours
Revised: January 7, 2014
Accepted: January 20, 2014
Published online: June 21, 2014
Processing time: 205 Days and 19.3 Hours
Core Tip
Core tip: The gut-liver axis has attracted much interest particularly regarding the pathogenesis of nonalcoholic fatty liver disease (NAFLD) because gut microbiota contribute to nutritional absorption and storage. In addition, gut microbiota are a source of Toll-like receptor (TLR) ligands, which can stimulate liver cells to produce proinflammatory cytokines. To date, TLR2, TLR4, TLR5, and TLR9 have been shown to be associated with the pathogenesis of NAFLD. The present article reviewed the current understanding of gut microbiota and TLR signaling in NAFLD and potential treatment targeted at gut microbiota and TLRs.