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沉默ANGPTL8减少了小鼠前脂肪细胞的分化和胰岛素信号传递

Anindya Ghosh¹, Yat Hei Leung¹, Jeffrey Yu²

¹Departments of Nutrition, Biochemistry and Molecular Medicine, University of Montreal, and Montreal Diabetes Research Center, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC, Canada.

Biochimica et biophysica acta. Molecular and cell biology of lipids

|January 25, 2024

概括

血管蛋白类8 (ANGPTL8) 在脂肪细胞分化和甘油三代谢中起着至关重要的细胞内作用. 它的淘汰会损害前脂肪细胞中的脂肪生成和胰岛素信号传递.

科学领域:

代谢调节代谢调节代谢调节
脂肪细胞生物学脂肪细胞生物学
分子内分泌学分子内分泌学

背景情况:

血管蛋白类8 (ANGPTL8) 主要以其在通过脂蛋白脂酶 (LPL) 活性调节甘油三代谢中的细胞外作用而闻名.
它的细胞内功能,特别是在像脂肪组织一样表达的组织中,仍然在很大程度上没有特征.

研究的目的:

研究ANGPTL8在脂肪细胞分化和功能中的细胞内作用.
确定ANGPTL8是否影响前脂肪细胞内的关键脂肪生成和胰岛素信号通路.

主要方法:

在小鼠初级皮下前脂肪细胞中使用siRNA. Knockdown的ANGPTL8表达.
评估脂肪细胞分化,甘油三积累和脂解.
RNA测序 (RNA-Seq) 分析,以分析在分化过程中的基因表达变化.
评估胰岛素介导的Akt酸化.

主要成果:

ANGPTL8的淘汰显著减少了脂肪细胞分化,细胞甘油三积累和脂解.
RNA-Seq显示,ANGPTL8的淘汰阻碍了基因 (例如,PPARγ) 和胰岛素信号基因的早期表达.
胰岛素介导的Akt酸化在脂肪细胞分化的早期阶段减少.

结论:

ANGPTL8在脂肪细胞内发挥细胞内作用,影响分化和新陈代谢.
预脂细胞ANGPTL8表达调节分化,可能通过胰岛素信号通路的改变.

关键词:

第八个角度脂肪细胞分化的差异化胰岛素的信号传递.PPARγ信号传递,脂肪生成通过RNA-Seq分析进行分析.

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