脂质代谢
过氧化物酶体增殖物激活受体
泛素
过氧化物酶体
脂肪变性
转录因子
肿瘤坏死因子α
β氧化
兴奋剂
受体
化学
新陈代谢
内分泌学
生物
生物化学
基因
作者
Ludivine Clavreul,Lucie Bernard,Alexia Cotte,Nathalie Hennuyer,Cyril Bourouh,Claire Devos,Audrey Helleboid,Joel T. Haas,An Verrijken,Céline Gheeraert,Bruno Derudas,Loïc Guille,Julie Chevalier,Jérôme Eeckhoute,Emmanuelle Vallez,Emilie Dorchies,Luc Van Gaal,Guillaume Lassailly,Sven Francque,Bart Staels,Réjane Paumelle
标识
DOI:10.1016/j.metabol.2023.155720
摘要
The ubiquitin-like modifier FAT10 is induced in MASLD and impairs the lipid regulatory activity of PPARα.In healthy hepatocytes, the transcriptional activity of Peroxisome Proliferator-Activated Receptor α (PPARα) is activated upon fasting by its natural ligands (i.e.fatty acids (FA)) or upon treatment by its synthetic agonist.In response, PPARα activates the transcription of FA oxidation-related genes, hence stimulating lipid metabolism.In Metabolic-dysfunction Associated Steatotic Liver Disease (MASLD), the ubiquitin-like modifier protein human leukocyte antigen-F Adjacent Transcript 10 (FAT10) is induced by pro-inflammatory stimuli (i.e.Interferon γ (IFNγ), Interleukin 6 (IL6) and Tumor Necrosis Factor α (TNFα)).FAT10 then interacts with PPARα, resulting in the inhibition of PPARα activation by its ligands.As a consequence, lipid metabolism and FA oxidation are impaired, and the accumulation of lipid droplets, steatosis and MASLD progression promoted.
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