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盐诱导性酶抑制促进脂肪细胞热生成程序和脂肪组织色

Fubiao Shi¹, Flaviane de Fatima Silva², Dianxin Liu¹

¹Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Molecular metabolism

|June 15, 2023

概括

盐诱导酶3 (SIK3) 作为一个关键的开关,在北上腺素刺激的热生成程序. 抑制SIK3促进脂肪组织的色,并可能为肥胖和心脏代谢疾病提供治疗益处.

科学领域:

细胞生物学细胞生物学
代谢过程中的代谢.
信号通道的信号通道

背景情况:

上腺素通过β-上腺素受体 (βAR) -cAMP-PKA通路激活脂肪组织热生成.
通过蛋白激酶A (PKA) 激活拉巴胺素复合体1 (mTORC1) 的机械标对于βAR刺激的脂肪组织色是必不可少的.
在发热过程中PKA-化mTORC1的下游机制尚不清楚.

研究的目的:

阐明PKA-mTORC1信号级联中的下游事件,驱动脂肪组织热生成.
在β-上腺刺激的背景下,识别mTORC1的新基质和调节剂.
为了研究盐诱导酶3 (SIK3) 在调节发热基因表达中的作用.

主要方法:

使用细胞培养中氨基酸 (SILAC) 通过/与氨基酸进行稳定同位素标记的蛋白质组分析,以分析棕色脂肪细胞中的蛋白质酸化.
通过基因淘汰 (shRNA) 和过度表达研究来研究SIK3的功能.
使用了SIK和mTORC1的药理抑制剂,以及CRISPR介导的基因删除.
评估了基因素脱乙酶 (HDAC) 活性和蛋白质乙化.

主要成果:

SIK3与mTORC1相互作用,并被PKA酸化.
抑制或缺乏SIK3可增强基底和βAR刺激的热生成基因表达 (例如Ucp1,Pgc1α).
通过CRISPR介导的Sik3删除增加了HDAC活性,并促进了发热基因表达.
在SIK抑制剂的体内给药刺激了小鼠的发热和脂肪组织色.

结论:

在β-上腺素介导的脂肪组织热生成中,SIK3作为关键的酸化依赖开关起作用.
针对SIKs为肥胖和相关心脏代谢疾病提供了潜在的治疗策略.
对SIK家族在温度调节中的作用进行进一步研究是有必要的.

关键词:

脂肪细胞脂肪细胞这就是SIK3的意义.盐诱导性激酶是一种盐诱导性激酶.热生成是一种热生成.在UCP1中,UCP1是UCP1.在 mTORC1 的情况下,mTORC1 是

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