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Endogenous catalase delays high-fat diet-induced liver injury in mice

Title
Endogenous catalase delays high-fat diet-induced liver injury in mice
Authors
Piao, LingjuanChoi, JiyeonKwon, GuideockHa, Hunjoo
Ewha Authors
하헌주
SCOPUS Author ID
하헌주scopus
Issue Date
2017
Journal Title
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
ISSN
1226-4512JCR Link2093-3827JCR Link
Citation
vol. 21, no. 3, pp. 317 - 325
Keywords
CatalaseInsulin resistanceNAFLDOxidative stressPeroxisome
Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Indexed
SCIE; SCOPUS; KCI WOS scopus
Abstract
Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease in parallel with worldwide epidemic of obesity. Reactive oxygen species (ROS) contributes to the development and progression of NAFLD. Peroxisomes play an important role in fatty acid oxidation and ROS homeostasis, and catalase is an antioxidant exclusively expressed in peroxisome. The present study examined the role of endogenous catalase in early stage of NAFLD. 8-week-old male catalase knock-out (CKO) and age-matched C57BL/6J wild type (WT) mice were fed either a normal diet (ND: 18% of total calories from fat) or a high fat diet (HFD: 60% of total calories from fat) for 2 weeks. CKO mice gained body weight faster than WT mice at early period of HFD feeding. Plasma triglyceride and ALT, fasting plasma insulin, as well as liver lipid accumulation, inflammation (F4/80 staining), and oxidative stress (8-oxo-dG staining and nitrotyrosine level) were significantly increased in CKO but not in WT mice at 2 weeks of HFD feeding. While phosphorylation of Akt (Ser473) and PGC1 alpha mRNA expression were decreased in both CKO and WT mice at HFD feeding, GSK3 beta phosphorylation and Cox4-il mRNA expression in the liver were decreased only in CKO-HF mice. Taken together, the present data demonstrated that endogenous catalase exerted beneficial effects in protecting liver injury including lipid accumulation and inflammation through maintaining liver redox balance from the early stage of HFD-induced metabolic stress.
DOI
10.4196/kjpp.2017.21.3.317
Appears in Collections:
약학대학 > 약학과 > Journal papers
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