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Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice

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Author(s)
Su-Kyung ShinHyun-Woo ChoSeung-Eun SongJae-Hoon BaeInha HwangHunjoo HaDae-Kyu SongSeung-Soon Im
Keimyung Author(s)
Bae, Jae HoonIm, Seung SoonSong, Dae Kyu
Department
Dept. of Physiology (생리학)
Journal Title
Pflügers Archiv - European Journal of Physiology
Issued Date
2019
Volume
471
Issue
6
Keyword
CatalaseOxidative stressNon-alcoholic fatty liver diseaseMitochondrial functionHydrogen peroxideErstress
Abstract
Hydrogen peroxide (H2O2) produced endogenously can cause mitochondrial dysfunction and metabolic complications in various cell types by inducing oxidative stress. In the liver, oxidative and endoplasmic reticulum (ER) stress affects the development of non-alcoholic fatty liver disease (NAFLD). Although a link between both stresses and fatty liver diseases has been suggested, few studies have investigated the involvement of catalase in fatty liver pathogenesis.We examined whether catalase is associated with NAFLD, using catalase knockout (CKO) mice and the catalase-deficient human hepatoma cell line HepG2. Hepatic morphology analysis revealed that the fat accumulation was more prominent in high-fat diet (HFD) CKO mice compared to that in agematched wild-type (WT) mice, and lipid peroxidation and H2O2 release were significantly elevated in CKO mice. Transmission electron micrographs indicated that the liver mitochondria fromCKO mice tended to be more severely damaged than those inWT mice. Likewise, mitochondrial DNA copy number and cellular ATP concentrations were significantly lower in CKO mice. In fatty acid-treated HepG2 cells, knockdown of catalase accelerated cellular lipid accumulation and depressed mitochondrial biogenesis, which was recovered by co-treatment with N-acetyl cysteine or melatonin. This effect of antioxidant was also true in HFD-fed CKO mice, suppressing fatty liver development and improving hepatic mitochondrial function. Expression of ER stress marker proteins and hepatic fat deposition also increased in normal-diet, aged CKO mice compared to WT mice. These findings suggest that H2O2 production may be an important event triggering NAFLD and that catalase may be an attractive therapeutic target for preventing NAFLD.
Keimyung Author(s)(Kor)
배재훈
임승순
송대규
Publisher
School of Medicine (의과대학)
Citation
Su-Kyung Shin et al. (2019). Ablation of catalase promotes non-alcoholic fatty liver via oxidative stress and mitochondrial dysfunction in diet-induced obese mice. Pflügers Archiv - European Journal of Physiology, 471(6), 829–843. doi: 10.1007/s00424-018-02250-3
Type
Article
ISSN
1432-2013
Source
https://link.springer.com/article/10.1007%2Fs00424-018-02250-3
DOI
10.1007/s00424-018-02250-3
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/41901
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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