Arginase Inhibition Ameliorates Hepatic Metabolic Abnormalities in Obese Mice
- Authors
- Moon, Jiyoung; Do, Hyun Ju; Cho, Yoonsu; Shin, Min-Jeong
- Issue Date
- 24-7월-2014
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.9, no.7
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLOS ONE
- Volume
- 9
- Number
- 7
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/97938
- DOI
- 10.1371/journal.pone.0103048
- ISSN
- 1932-6203
- Abstract
- Objectives: We examined whether arginase inhibition influences hepatic metabolic pathways and whole body adiposity in diet-induced obesity. Methods and Results: After obesity induction by a high fat diet (HFD), mice were fed either the HFD or the HFD with an arginase inhibitor, N-omega-hydroxy-nor-L-arginine (nor-NOHA). Nor-NOHA significantly prevented HFD-induced increases in body, liver, and visceral fat tissue weight, and ameliorated abnormal lipid profiles. Furthermore, nor-NOHA treatment reduced lipid accumulation in oleic acid-induced hepatic steatosis in vitro. Arginase inhibition increased hepatic nitric oxide (NO) in HFD-fed mice and HepG2 cells, and reversed the elevated mRNA expression of hepatic genes in lipid metabolism. Expression of phosphorylated 5' AMPK-activated protein kinase alpha was increased by arginase inhibition in the mouse livers and HepG2 cells. Conclusions: Arginase inhibition ameliorated obesity-induced hepatic lipid abnormalities and whole body adiposity, possibly as a result of increased hepatic NO production and subsequent activation of metabolic pathways involved in hepatic triglyceride metabolism and mitochondrial function.
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Collections - College of Health Sciences > School of Biosystems and Biomedical Sciences > 1. Journal Articles
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