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在人类脂肪细胞中,cAMP驱动的UCP1诱导需要ATGL催化脂解

Anand Desai¹, Zinger Yang Loureiro², Tiffany DeSouza¹

¹Program in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.

Molecular metabolism

|October 25, 2024

概括

罗西格利塔 (Rsg) 和佛斯科林 (Fsk) 在人体脂肪细胞中急性诱导解蛋白1 (UCP1). 对于最大的cAMP诱导的UCP1表达,需要ATGL介导的脂解,这表明脂解和PPARγ激活之间存在联系.

科学领域:

细胞生物学细胞生物学
代谢过程中的代谢.
内分泌学在内分泌学.

背景情况:

解蛋白1 (UCP1) 是棕色/色脂肪细胞热生成的关键,由cAMP信号诱导.
像rosiglitazone (Rsg) 这样的PPARγ激动剂也增强了UCP1,但其在现有的脂肪细胞和新分化的诱导机制尚不清楚.

研究的目的:

研究Rsg和福斯科林 (Fsk) 对人类脂肪细胞中UCP1表达的急性影响.
为了确定RSG诱导的UCP1上调是否涉及新的色脂肪细胞分化或成熟脂肪细胞的直接诱导.

主要方法:

从原始细胞分化的人类脂肪细胞被用Fsk,Rsg或两者一起治疗.
这些技术包括批量RNASeq,RNAScope,RT-PCR,CRISPR-Cas9对PNPLA2 (ATGL) 的淘汰,氧气消耗和西部涂抹.

主要成果:

无论是Rsg还是Fsk都迅速诱导了UCP1mRNA,独立于新的脂肪细胞分化.
通过ATGL淘汰赛,FSK诱导的UCP1显著减少,这表明脂解对于cAMP介导的UCP1诱导至关重要.
Rsg治疗逆转了ATGL淘汰诱导的FSK刺激的UCP1抑制,这表明脂解产生天然PPARγ激动剂.

结论:

在人类脂肪细胞中,UCP1转录通过cAMP依赖的途径和PPARγ激活都被急性诱导.
通过cAMP信号,可以通过这两种途径协同增强UCP1表达.
通过ATGL介导的脂解可能会产生激活PPARγ的配体,从而促进cAMP诱导的UCP1表达.

关键词:

色的脂肪脂肪是什么棕色的脂肪脂肪是什么卡特科拉胺是什么类型的激素信号传递的激素.天然的连接物是天然的连接物核受体是核受体的一个组成部分.热生成是一种热生成.

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