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Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPAR delta Regulation in Hyperlipidemic and Hypertensive Conditionsopen access

Authors
Lee, Yong-JikJang, Yoo-NaHan, Yoon-MiKim, Hyun-MinJeong, Jong-MinSeo, Hong Seog
Issue Date
Mar-2017
Publisher
Hindawi Publishing Corporation
Citation
PPAR Research, v.2017
Indexed
SCIE
SCOPUS
Journal Title
PPAR Research
Volume
2017
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/5678
DOI
10.1155/2017/8048720
ISSN
1687-4757
1687-4765
Abstract
To investigate the effects of fimasartan on nonalcoholic fatty liver disease in hyperlipidemic and hypertensive conditions, the levels of biomarkers related to fatty acid metabolism were determined in HepG2 and differentiated 3T3-L1 cells treated by high fatty acid and liver and visceral fat tissue samples of spontaneously hypertensive rats (SHRs) given high-fat diet. In HepG2 cells and liver tissues, fimasartan was shown to increase the protein levels of peroxisome proliferator-activated receptor delta (PPAR delta), phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK), phosphorylated acetyl-CoA carboxylase (p-ACC), malonyl-CoA decarboxylase (MCD), medium chain acyl-CoA dehydrogenase (MCAD), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha), and it led to a decrease in the protein levels of 11 beta-hydroxysteroid dehydrogenase 1 (11 beta-HSDH1), fatty acid synthase (FAS), and tumor necrosis factor-alpha (TNF-alpha). Fimasartan decreased lipid contents in HepG2 and differentiated 3T3-L1 cells and liver tissues. In addition, fimasartan increased the adiponectin level in visceral fat tissues. The antiadipogenic effects of fimasartan were offset by PPAR delta antagonist (GSK0660). Consequently, fimasartan ameliorates nonalcoholic fatty liver disease mainly through the activation of oxidative metabolism represented by PPAR delta-AMPK-PGC-1. pathway.
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Guro Hospital (Department of Cardiology, Guro Hospital)
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