Lipoic Acid Prevents the Changes of Intracellular Lipid Partitioning by Free Fatty Acid.
- Author:
Dong Chan KIM
1
;
Dae Won JUN
;
Eun Chul JANG
;
Sang Heum KIM
;
Eun Kyung KIM
;
Sang Pyo LEE
;
Kang Nyeong LEE
;
Hang Lak LEE
;
Oh Young LEE
;
Byung Chul YOON
;
Ho Soon CHOI
Author Information
1. Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. noshin1004@google.co.kr
- Publication Type:Original Article
- Keywords:
Thioctic acid;
Lipotoxicity;
Lipid partitioning;
Non-alcoholic steatohepatitis;
Liver cirrhosis
- MeSH:
Apoptosis;
Cell Membrane;
Cholesterol;
Coat Protein Complex I;
DNA, Mitochondrial;
Fatty Liver;
Fluorescence;
Hep G2 Cells;
Liver Cirrhosis;
Palmitic Acid;
Reactive Oxygen Species;
Thioctic Acid
- From:Gut and Liver
2013;7(2):221-227
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: It is suggested that the hepatic lipid composition is more important than lipid quantity in the pathogenesis of non-alcoholic steatohepatitis. We examined whether lipoic acid (LA) could alter intrahepatic lipid composition and free cholesterol distribution. METHODS: HepG2 cells were cultured with palmitic acid (PA) with and without LA. Apoptosis, changes of the mitochondrial structure, intracellular lipid partitioning, and reactive oxygen species (ROS) activity were measured. RESULTS: Free fatty acid (FA) increased apoptosis, and LA co-treatment prevented this lipotoxicity (apoptosis in controls vs PA vs PA+LA, 0.5% vs 19.5% vs 1.6%, p<0.05). LA also restored the intracellular mitochondrial DNA copy number (553+/-33.8 copies vs 291+/-14.55 copies vs 421+/-21.05 copies, p<0.05) and reversed the morphological changes induced by PA. In addition, ROS was increased in response to PA and was decreased in response to LA co-treatment (41,382 relative fluorescence unit [RFU] vs 43,646 RFU vs 41,935 RFU, p<0.05). LA co-treatment increased the monounsaturated and polyunsaturated FA concentrations and decreased the total saturated FA fraction. It also prevented the movement of intracellular free cholesterol from the cell membrane to the cytoplasm. CONCLUSIONS: LA opposes free FA-generated lipotoxicity by altering the intracellular lipid composition and free cholesterol distribution.
