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Fas-Associated Factor 1 Promotes Hepatic Insulin Resistance via JNK Signaling Pathway(Open Access)

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机构： [1]Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410078, China [2]Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha 410011, China [3]Institute of Clinical Pharmacy, Central South University, Changsha 410011, China [4]Institute of Clinical Medicine, The First Affiliated Hospital, University of South China, Hengyang 421001, China [5]Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, Changsha 410078, China [6]Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha 410078, China [7]National Clinical Research Center for Geriatric Disorders, Changsha 410008, China [8]Zhuhai People’s Hospital (Zhuhai Hospital Affiliated with Jinan University), Zhuhai 519000, China [9]Department of Laboratory Medicine, National Key Laboratory of Biotherapy/Collaborative Innovation Center of Biotherapy andCancer Center, West China Hospital, Sichuan University, Chengdu 610041, China [10]Department of Gastrointestinal Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China

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Fas-associated factor 1 (FAF1), a member of the Fas death-inducing signaling complex, is reported to interact potentially with diverse proteins and function in diverse cellular possesses. It remains unclear, however, whether FAF1 is involved in hepatic metabolic disorder and insulin resistance. This study is aimed at elucidating the role and the molecular mechanism of FAF1 in hepatic insulin resistance. Rats treated with high-fat diets are used as hepatic insulin resistance animal models. Quantitative real-time PCR, immunohistochemistry, and immunofluorescence assay are utilized to detect the FAF1 expression. The expression of relevant proteins is detected by Western blotting. We determine ROS production, lipid accumulation, and glucose uptake by using flow cytometry. Immunoprecipitation is employed to investigate protein-protein interaction. We find that increased expression of FAF1 occurred in the livers of insulin-resistant rats. Using gain-of-function and loss-of-function approaches, we observe dramatic exacerbation of insulin resistance, upregulated gluconeogenesis genes, downregulated glucose transport genes, and enhanced ROS production by FAF1 overexpression, whereas downregulation of FAF1 leads to a completely opposite phenotype. Mechanistically, FAF1 interacts directly with c-Jun N-terminal kinase (JNK) and activates its phosphorylation, thereby blocking the downstream insulin signaling pathway and leading to insulin resistance. Our data indicate that FAF1 is a potent regulator in hepatic metabolic disorder and insulin resistance. © 2021 Bao Sun et al.

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大类 | 2 区生物学

小类 | 3 区细胞生物学

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Q2 CELL BIOLOGY

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影响因子： 0 最新[2023版] 0 最新五年平均 7.31 出版当年[2021版] 8.427 出版当年五年平均 6.543 出版前一年[2020版]

第一作者：

第一作者机构： [1]Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410078, China [2]Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha 410011, China [3]Institute of Clinical Pharmacy, Central South University, Changsha 410011, China

通讯作者：

通讯机构： [1]Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410078, China [5]Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, Changsha 410078, China [6]Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha 410078, China [7]National Clinical Research Center for Geriatric Disorders, Changsha 410008, China

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