非酒精性脂肪肝病（NAFLD）因其逐年升高的患病率而日益受到重视。线粒体三功能蛋白α（MTPα）是催化脂肪酸β氧化第二、三步反应的酶。MTPα基因敲除的小鼠出现NAFLD、胰岛素抵抗等代谢异常。乙酰化则是调节代谢酶功能的一种重要的翻译后修饰。然而目前还鲜有关于MTPα乙酰化的研究报道。我们的前期研究发现：1) MTPα存在乙酰化，并且 MTPα的乙酰化可以提高其蛋白稳定性;2) NAFLD的个体（小鼠、人）肝脏中MTPα的蛋白水平显著低于对照的个体，而MTPα的mRNA水平没有显著差异。本项目将基于前期基础，结合分子生物学实验、NAFLD动物模型以及临床NAFLD样本的检测，研究MTPα的乙酰化影响MTPα蛋白稳定性的分子机制，并探寻其在NAFLD发生、发展中的作用。该研究将为NAFLD发病机制的阐明奠定基础，并为人们寻找干预NAFLD的分子靶点，制定更为合理的临床诊疗方案提供新的思路。

More importance has been attached to Non-alcoholic Fatty Liver Disease (NAFLD) owing to its increased morbidity rate. Mitochondrial Trifunctional Protein α (MTPα) catalyzes the second and third steps of fatty acid β-oxidation. MTPα +/- mice display metabolic disorders, such as NAFLD and Insulin Resistance. Acetylation is an important Post-translational Modification (PTM) regulating the function of metabolic enzymes. However, no research on the acetylation of MTPα has been reported. In our previous studies, we found 1) MTPα is modified by acetylation and the acetylation of MTPα increases its protein stability; 2) In the livers of NAFLD individuals, the protein level of MTPα is significantly lower than that in the livers of control individuals, while no significant difference is detected in its mRNA level. Based on these results obtained previously, we will combine the experimental methods of molecular biology, animal models and clinical samples examination, to further investigate the role and mechanism of MTPα acetylation in NAFLD. These studies might deepen our understanding of the molecular mechanism of NAFLD, help to identify new therapeutic target and contribute to making more reasonable schemes to diagnose and treat NAFLD patients.