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ACSL1 正向调控脂肪生成分化。

ACSL1 positively regulates adipogenic differentiation.

机构信息

Wuxi School of Medicine, Jiangnan University, Wuxi, 214000, China.

Wuxi School of Medicine, Jiangnan University, Wuxi, 214000, China; The Second School of Clinical Medical, Xuzhou Medical University, Xuzhou, Jiangsu, China.

出版信息

Biochem Biophys Res Commun. 2024 Nov 26;735:150865. doi: 10.1016/j.bbrc.2024.150865. Epub 2024 Oct 21.

DOI:10.1016/j.bbrc.2024.150865
PMID:39442449
Abstract

Aberrant adipogenic differentiation is strongly associated with obesity and related metabolic diseases. Elucidating the key factors driving adipogenesis is an effective strategy for identifying novel therapeutic targets for treating metabolic diseases represented by obesity. In this study, transcriptomic techniques were employed to investigate the functional genes that regulate adipogenic differentiation in OP9 cells and 3T3-L1 cells. The findings indicated a notable upregulation of Acsl1 expression throughout the adipogenic differentiation process. Knocking down Acsl1 led to a decrease in the expression of genes associated with adipogenesis and a reduction in triglyceride accumulation. Additionally, Acsl1 overexpression promoted adipocyte differentiation and adipose-specific overexpression of Acsl1 markedly aggravated steatosis induced by a high-fat diet. Mechanistically, Cyp2f2, Dusp23 and Gstm2 are the crucial genes implicated in Acsl1-induced adipogenic differentiation. The findings of this study indicate that Acsl1 promotes adipogenesis and could serve as a potential therapeutic target for treating obesity and related metabolic disorders.

摘要

脂肪生成分化异常与肥胖和相关代谢性疾病密切相关。阐明驱动脂肪生成的关键因素是鉴定肥胖为代表的代谢性疾病的新型治疗靶点的有效策略。在这项研究中,采用转录组学技术研究了调节 OP9 细胞和 3T3-L1 细胞脂肪生成分化的功能基因。研究结果表明,Acsl1 在整个脂肪生成分化过程中的表达显著上调。敲低 Acsl1 导致与脂肪生成相关的基因表达减少和甘油三酯积累减少。此外,Acsl1 的过表达促进脂肪细胞分化,脂肪特异性过表达 Acsl1 显著加重高脂肪饮食诱导的脂肪变性。在机制上,Cyp2f2、Dusp23 和 Gstm2 是 Acsl1 诱导的脂肪生成分化中涉及的关键基因。本研究结果表明,Acsl1 促进脂肪生成,可作为治疗肥胖和相关代谢紊乱的潜在治疗靶点。

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