دورية أكاديمية

CSAD Ameliorates Lipid Accumulation in High-Fat Diet-Fed Mice

التفاصيل البيبلوغرافية
العنوان: CSAD Ameliorates Lipid Accumulation in High-Fat Diet-Fed Mice
المؤلفون: Rongrong Tan, Jiayang Li, Lu Liu, Qian Wu, Lei Fan, Ningning Ma, Chuwei Yu, Henglei Lu, Xuemei Zhang, Jing Chen, Likun Gong, Jin Ren
المصدر: International Journal of Molecular Sciences, Vol 23, Iss 24, p 15931 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: NAFLD, CSAD, obesity, liver damage, fatty acid β-oxidation, mitochondrial damage, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic disease manifested in hepatic steatosis, inflammation, fibrosis, etc., which affects over one-quarter of the population around the world. Since no effective therapeutic drugs are available to cope with this widespread epidemic, the functional research of genes with altered expression during NAFLD helps understand the pathogenesis of this disease and the development of new potential therapeutic targets for drugs. In the current work, we discovered via the analysis of the Gene Expression Omnibus (GEO) dataset that cysteine sulfinic acid decarboxylase (CSAD) decreased significantly in NAFLD patients, which was also confirmed in multiple NAFLD mouse models (HFD-fed C57BL/6J, db/db and HFHFrHC-fed C57BL/6J mice). Next, CSAD’s function in the progression of NAFLD was explored using AAV-mediated liver-directed gene overexpression in an HFD-fed mouse model, where the overexpression of CSAD in the liver could alleviate NAFLD-associated pathologies, including body weight, liver/body weight ratio, hepatic triglyceride and total cholesterol, and the degree of steatosis. Mechanically, we found that the overexpression of CSAD could increase the expression of some genes related to fatty acid β-oxidation (Acad1, Ppara, and Acox1). Furthermore, we also detected that CSAD could improve mitochondrial injury in vitro and in vivo. Finally, we proposed that the effect of CSAD on lipid accumulation might be independent of the taurine pathway. In conclusion, we demonstrated that CSAD is involved in the development of NAFLD as a protective factor, which suggested that CSAD has the potential to become a new target for drug discovery in NAFLD.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
1661-6596
العلاقة: https://www.mdpi.com/1422-0067/23/24/15931Test; https://doaj.org/toc/1661-6596Test; https://doaj.org/toc/1422-0067Test
DOI: 10.3390/ijms232415931
الوصول الحر: https://doaj.org/article/abbfca96e6114926a3684f716cf0953fTest
رقم الانضمام: edsdoj.bbfca96e6114926a3684f716cf0953f
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
16616596
DOI:10.3390/ijms232415931