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ID 116735
Author
Azuma, Yasu-Taka Osaka Prefecture University
Fujita, Takashi Ritsumeikan University
Izawa, Takeshi Osaka Prefecture University
Hirota, Kana Osaka Prefecture University
Nishiyama, Kazuhiro Osaka Prefecture University
Ikegami, Airi Ritsumeikan University
Aoyama, Tomoko Ritsumeikan University
Ike, Mikihito Ritsumeikan University
Ushikai, Yumi Osaka Prefecture University
Kuwamura, Mitsuru Osaka Prefecture University
Fujii, Hideki Osaka City University
Keywords
IL-19
NAFLD
NASH
inflammation
liver
lipogenesis
Content Type
Journal Article
Description
Interleukin (IL)-19, a member of the IL-10 family, is an anti-inflammatory cytokine produced primarily by macrophages. Nonalcoholic steatohepatitis (NASH) is a disease that has progressed from nonalcoholic fatty liver disease (NAFLD) and is characterized by inflammation and fibrosis. We evaluated the functions of IL-19 in a NAFLD/NASH mouse model using a 60% high fat diet with 0.1% methionine, without choline, and with 2% cholesterol (CDAHFD). Wild-type (WT) and IL-19 gene-deficient (KO) mice were fed a CDAHFD or standard diet for 9 weeks. Liver injury, inflammation, and fibrosis induced by CDAHFD were significantly worse in IL-19 KO mice than in WT mice. IL-6, TNF-α, and TGF-β were significantly higher in IL-19 KO mice than in WT mice. As a mechanism using an in vitro experiment, palmitate-induced triglyceride and cholesterol contents were decreased by the addition of IL-19 in HepG2 cells. Furthermore, addition of IL-19 decreased the expression of fatty acid synthesis-related enzymes and increased ATP content in HepG2 cells. The action of IL-19 in vitro suppressed lipid metabolism. In conclusion, IL-19 may play an important role in the development of steatosis and fibrosis by directly regulating liver metabolism and may be a potential target for the treatment of liver diseases.
Journal Title
Cells
ISSN
20734409
Publisher
MDPI
Volume
10
Issue
12
Start Page
3513
Published Date
2021-12-13
Rights
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
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DOI (Published Version)
URL ( Publisher's Version )
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language
eng
TextVersion
Publisher
departments
Medical Sciences