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TM4SF5-mediated abnormal food-intake behavior and apelin expression facilitate non-alcoholic fatty liver disease features
- Title
- TM4SF5-mediated abnormal food-intake behavior and apelin expression facilitate non-alcoholic fatty liver disease features
- Authors
- Pinanga, Yangie Dwi; Lee, Han Ah; Shin, Eun-Ae; Lee, Haesong; Pyo, Kyung-hee; Kim, Ji Eon; Lee, Eun Hae; Kim, Wonsik; Kim, Soyeon; Kim, Hwi Young; Weon, Jung
- Ewha Authors
- 김휘영; 이한아
- SCOPUS Author ID
- 김휘영; 이한아
- Issue Date
- 2023
- Journal Title
- ISCIENCE
- ISSN
- 2589-0042
- Citation
- ISCIENCE vol. 26, no. 9
- Publisher
- CELL PRESS
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- Abstract
- Transmembrane 4 L six family member 5 (TM4SF5) engages in non-alcoholic steatohepatitis (NASH), although its mechanistic roles are unclear. Genetically engineered Tm4sf5 mice fed ad libitum normal chow or high-fat diet for either an entire day or a daytime-feeding (DF) pattern were analyzed for metabolic parameters. Compared to wild-type and Tm4sf5(-/-) knockout mice, hepatocyte-specific TM4SF5-overexpressing Alb-TG(Tm4sf5-Flag) (TG) mice showed abnormal food-intake behavior during the mouse-inactive daytime, increased apelin expression, increased food intake, and higher levels of NASH features. DF or exogenous apelin injection of TG mice caused severe hepatic pathology. TM4SF5-mediated abnormal food intake was correlated with peroxisomal beta-oxidation, mTOR activation, and autophagy inhibition, with triggering NASH phenotypes. Non-alcoholic fatty liver disease (NAFLD) patients' samples revealed a correlation between serum apelin and NAFLD activity score. Altogether, these observations suggest that hepatic TM4SF5 may cause abnormal food-intake behaviors to trigger steatohepatitic features via the regulation of peroxisomal beta-oxidation, mTOR, and autophagy.
- DOI
- 10.1016/j.isci.2023.107625
- Appears in Collections:
- 의과대학 > 의학과 > Journal papers
- Files in This Item:
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