J Clin Invest：科学家发现通过表观遗传减脂的重要分子

2018-06-23 佚名细胞

组蛋白去甲基化酶JMJD3能够在表观遗传修饰水平调控发育和分化、免疫以及肿瘤发生过程，该分子能够对具有基因抑制性作用的组蛋白标记H3K27-me3进行去甲基化，但是JMJD3在代谢调节方面的作用还没有得到深入研究。最近来自美国的研究人员在国际学术期刊JCI上发表了一项最新研究进展，他们发现JMJD3能够在饥饿情况下促进β氧化过程降低脂质水平。

组蛋白去甲基化酶JMJD3能够在表观遗传修饰水平调控发育和分化、免疫以及肿瘤发生过程，该分子能够对具有基因抑制性作用的组蛋白标记H3K27-me3进行去甲基化，但是JMJD3在代谢调节方面的作用还没有得到深入研究。最近来自美国的研究人员在国际学术期刊JCI上发表了一项最新研究进展，他们发现JMJD3能够在饥饿情况下促进β氧化过程降低脂质水平。

去乙酰化酶SIRT1能够在饥饿情况下直接激活与肝脏糖异生和线粒体脂肪酸β氧化有关的基因，但隐藏其中的表观遗传和基因特异性机制仍然不清楚。在这项研究中，研究人员发现JMJD3是SIRT1的基因特异性转录合作伙伴，在饥饿情况下能够在表观遗传修饰水平激活线粒体β氧化相关基因的表达，但是不会影响糖异生相关基因。

从机制上来说，研究人员发现JMJD3与SIRT1和核受体PPARa形成一个正向自调控回路，调节饥饿诱导的PKA信号途径，并在表观遗传修饰水平激活与β氧化相关的基因，包括Fgf21，Cpt1a和Mcad。肝脏特异性下调JMJD3会导致β氧化过程的损伤，促进肝脏脂肪浸润以及葡萄糖和胰岛素不耐受的情况发生。值得注意的是，JMJD3或SIRT1对饮食诱导肥胖小鼠发挥的降脂作用是相互依赖的。

研究人员认为JMJD3组蛋白去甲基化酶或可作为一个药物靶点用于肥胖、脂肪肝和2型糖尿病的治疗，特异性降低脂质水平同时不会引起血糖水平的升高。

原始出处：

Seok S, Kim YC, Byun S, et al.Fasting-induced JMJD3 histone demethylase epigenetically activates mitochondrial fatty acid β-oxidation.J Clin Invest. 2018 Jun 18. pii: 97736. doi: 10.1172/JCI97736. [Epub ahead of print]

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2019-02-12 xiangyuzhou971

#EST#

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2019-03-21 旅苦化文_208

#科学家发现#

67 0
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2019-01-23 gdsun

#重要分子#

64 0
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2018-06-25 lujian

#减脂#

59 0
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2018-06-24 zb1235672

好消息!!!!!

87 0
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2018-06-23 131****1460

学习了受益匪浅

100 0
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2018-06-23 kafei

学习学习谢谢

107 0
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2018-06-23 天地飞扬

了解一下.谢谢分享!

115 0
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2018-06-23 医者仁心5538

学习了

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