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Catalase and nonalcoholic fatty liver disease

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Author(s)
Su-Kyung ShinHyun-Woo ChoSeung-Eun SongDae-Kyu Song
Keimyung Author(s)
Song, Dae Kyu
Department
Dept. of Physiology (생리학)
Journal Title
Pflügers Archiv - European Journal of Physiology
Issued Date
2018
Volume
470
Issue
20
Abstract
Obesity and insulin resistance are considered the main causes of nonalcoholic fatty liver disease (NAFLD), and oxidative stress accelerates the progression of NAFLD. Free fatty acids, which are elevated in the liver by obesity or insulin resistance, lead to incomplete oxidation in the mitochondria, peroxisomes, and microsomes, leading to the production of reactive oxygen species (ROS). Among the ROS generated, H2O2 is mainly produced in peroxisomes and decomposed by catalase. However, when the H2O2 concentration increases because of decreased expression or activity of catalase, it migrates to cytosol and other organelles, causing cell injury and participating in the Fenton reaction, resulting in serious oxidative stress. To date, numerous studies have been shown to inhibit the pathogenesis of NAFLD, but treatment for this disease mainly depends on weight loss and exercise. Various molecules such as vitamin E, metformin, liraglutide, and resveratrol have been proposed as therapeutic agents, but further verification of the dose setting, clinical application, and side effects is needed. Reducing oxidative stress may be a fundamental method for improving not only the progression of NAFLD but also obesity and insulin resistance. However, the relationship between NAFLD progression and antioxidants, particularly catalase, which is most commonly expressed in the liver, remains unclear. Therefore, this review summarizes the role of catalase, focusing on its potential therapeutic effects in NAFLD progression.
Keimyung Author(s)(Kor)
송대규
Publisher
School of Medicine (의과대학)
Citation
Su-Kyung Shin et al. (2018). Catalase and nonalcoholic fatty liver disease. Pflügers Archiv - European Journal of Physiology, 470(20), 1721–1737. doi: 10.1007/s00424-018-2195-z
Type
Article
ISSN
1432-2013
Source
https://link.springer.com/article/10.1007%2Fs00424-018-2195-z
DOI
10.1007/s00424-018-2195-z
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/41759
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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