相关实验视频

Updated: May 11, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

在KLF9mRNA中NAT10介导的N4-乙基胺修饰促进了脂肪生成

Xinxing Wan¹, Linghao Wang¹, Md Asaduzzaman Khan²

¹Department of Endocrinology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, PR China.

Cell death and differentiation

|March 24, 2025

概括

N-乙转移酶10 (NAT10) 通过增强脂肪生成和KLF9 mRNA稳定性来促进肥胖. 抑制NAT10可以降低体重和脂肪组织扩张,提供潜在的肥胖治疗方法.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
代谢疾病代谢疾病

背景情况:

功能障碍脂肪生成是导致肥胖的一个关键因素.
N-乙转移酶10 (NAT10) 调节RNA修饰 (ac4C),影响mRNA的稳定性和翻译.
NAT10在脂肪生成和肥胖中的作用在很大程度上仍未被探索.

研究的目的:

研究NAT10在脂肪生成和肥胖中的作用.
为了确定NAT10的下游目标和脂肪组织中的分子机制.
评估NAT10作为肥胖的潜在治疗标.

主要方法:

在肥胖个体和小鼠中分析NAT10表达.
在人类脂肪组织衍生干细胞 (hADSCs) 和3T3-L1细胞中进行过度表达和沉默研究.
结合acRIP测序 (acRIP-seq) 和RNA测序 (RNA-seq) 来识别NAT10的目标.
通过acRIP-PCR,双露西法酶记者测定,以及使用AAV-NAT10和NAT10抑制剂 (Remodelin) 的体内研究.

主要成果:

在肥胖者和小鼠的脂肪组织中,NAT10的高调显著.
过度表达NAT10促进脂肪生成,而沉默则抑制了它.
NAT10增强了KLF9mRNA的稳定性,并激活了CEBPA/B-PPARG通路.
NAT10 直接与 KLF9 的 mRNA 基因结合.
在体内抑制NAT10 (AAV-shRNA-mNAT10或Remodelin) 减少了饮食诱导的肥胖小鼠的脂肪组织扩张和体重.

结论:

NAT10在促进脂肪生成和肥胖方面发挥着至关重要的作用.
NAT10通过KLF9mRNA稳定和随后的途径激活来调节脂肪生成.
针对NAT10及其下游影响者,为预防和治疗肥胖症提供了一个有前途的治疗策略.

更多相关视频

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

Adipocyte-Specific ATAC-Seq with Adipose Tissues Using Fluorescence-Activated Nucleus Sorting

Adipocyte-Specific ATAC-Seq with Adipose Tissues Using Fluorescence-Activated Nucleus Sorting

Published on: March 17, 2023

相关概念视频

Lipid Catabolism

Lipid Catabolism

Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...