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CLCF1通过抑制棕色脂肪热生成来抑制能量消耗

Youwen Yuan^1,2,3, Kangli Li⁴, Xueru Ye^1,2,3

¹Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Proceedings of the National Academy of Sciences of the United States of America

|January 8, 2024

概括

心脏类型细胞因子1 (CLCF1) 抑制棕色脂肪 (BAT) 的热生成. 阻止CLCF1可提高BAT功能,提高能源消耗,并防止肥胖,提供潜在的治疗点.

科学领域:

代谢调节代谢调节代谢调节
脂肪组织生物学脂肪组织生物学
热生成是一种热生成.

背景情况:

棕色脂肪组织 (BAT) 对于发热和能量代谢至关重要.
抑制BAT活动的监管因素在很大程度上是未知的.
了解这些因素是代谢健康的关键.

研究的目的:

在棕色脂肪组织中识别新型的热生成负调节剂.
调查心肌类型细胞因子1 (CLCF1) 在BAT功能中的作用.
探索CLCF1作为代谢障碍的潜在治疗点.

主要方法:

以腺病毒为媒介的基因操纵来改变BAT中的CLCF1水平.
评估BAT热能能力和新陈代谢率.
对下游信号通路的分析,包括ADCY3和PERK-ATF4.4.
对抗饮食引起的肥胖和代谢功能障碍的保护的评估.

主要成果:

鉴定出心心类细胞因子1 (CLCF1) 是BAT热生成的负调节者.
过度表达CLCF1损害了BAT功能,而其切除则增强了发热和能源消耗.
CLCF1通过PERK-ATF4通路负面调节ADCY3转录.
删除CLCF1保护小鼠免受饮食诱导的肥胖和改善的葡萄糖/脂质代谢.

结论:

CLCF1在抑制BAT热生成方面发挥着至关重要的作用.
抑制CLCF1信号传递可能是治疗肥胖和相关代谢疾病的治疗策略.
准CLCF1提供了一种新的方法来提高能源消耗和打击代谢功能障碍.

关键词:

在CLCF1中,棕色脂肪组织棕色脂肪组织肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖热生成是一种热生成.

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