Hu J, Hong W, Yao KN, Zhu XH, Chen ZY, Ye L. Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway. World J Gastroenterol 2019; 25(12): 1492-1501 [PMID: 30948912 DOI: 10.3748/wjg.v25.i12.1492]
Corresponding Author of This Article
Lei Ye, MAMS, Doctor, Department of Infectious Diseases, The First Affiliated Hospital of Zhejiang Chinese Medical University, No. 54, Youdian Road, Hangzhou 310006, Zhejiang Province, China. huj520@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
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/
World J Gastroenterol. Mar 28, 2019; 25(12): 1492-1501 Published online Mar 28, 2019. doi: 10.3748/wjg.v25.i12.1492
Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway
Jie Hu, Wei Hong, Kan-Nan Yao, Xiao-Hong Zhu, Zhi-Yun Chen, Lei Ye
Jie Hu, Xiao-Hong Zhu, Lei Ye, Department of Infectious Diseases, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, Zhejiang Province, China
Wei Hong, Kan-Nan Yao, Zhi-Yun Chen, the Second Central Laboratory, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, Zhejiang Province, China
Author contributions: Hu J and Ye L designed the research; Yao KN and Hong W performed the research; Chen ZY and Zhu XH contributed new reagents or analytic tools; Yao KN and Chen ZY analyzed the data; Hu J and Hong W wrote the paper.
Supported bythe Natural Science Foundation of Zhejiang Province, China, No. LQ19H290001.
Conflict-of-interest statement: There is no conflict of interest in this study.
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/
Corresponding author: Lei Ye, MAMS, Doctor, Department of Infectious Diseases, The First Affiliated Hospital of Zhejiang Chinese Medical University, No. 54, Youdian Road, Hangzhou 310006, Zhejiang Province, China. huj520@163.com
Telephone: +86-571-86919345 Fax: +86-571-86919345
Received: November 27, 2018 Peer-review started: November 27, 2018 First decision: January 11, 2019 Revised: January 29, 2019 Accepted: January 30, 2019 Article in press: January 30, 2019 Published online: March 28, 2019 Processing time: 121 Days and 22.7 Hours
Core Tip
Core tip: Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease. Many studies show that the disorder of hepatic lipid metabolism is the major pathogenesis. Increased evidence indicates that the AKT/mTOR/SREBP-1 signaling pathway is a key pathway to regulate hepatocellular lipid metabolism. At present, there are few studies on the mechanism of NAFLD with regard to hepatic lipid metabolism. We aimed to investigate the functional mechanism of ursodeoxycholic acid (UDCA) in the oleic acid-induced cellular model of NAFLD. The possible molecular mechanism and related targets of regulating hepatic lipid metabolism were explored, and the correlation between the occurrence of NAFLD and the AKT/mTOR/SREBP-1 signaling pathway was explored. We provided more sufficient experimental basis for clinical application of UDCA in the treatment of NAFLD.
