JMJD8通过与脂肪周蛋白2相互作用调节脂肪细胞肥大。
JMJD8 Regulates Adipocyte Hypertrophy Through the Interaction With Perilipin 2.
作者信息
You Dongjoo, Kang Sona
机构信息
Nutritional Sciences and Toxicology Department, University of California, Berkeley, Berkeley, CA.
出版信息
Diabetes. 2025 Apr 1;74(4):458-471. doi: 10.2337/db23-0883.
Abstract
New research builds on previous findings that JMJD8 mediates insulin resistance by promoting adipocyte hypertrophy. We identified PLIN2 as a binding partner of JMJD8 using proteomics approaches. This study reveals a physical interaction between JMJD8 and PLIN2, which plays a crucial role in driving adipocyte hypertrophy and insulin resistance. JMJD8 suppresses fasting-induced lipophagy and reduces energy production by inhibiting PLIN2 phosphorylation. These findings highlight the importance of JMJD8 and PLIN2 in regulating lipid droplet homeostasis and suggest a potential mechanism for controlling fat mobilization during energy deprivation.
摘要
新的研究基于之前的发现，即JMJD8通过促进脂肪细胞肥大介导胰岛素抵抗。我们使用蛋白质组学方法将PLIN2鉴定为JMJD8的结合伴侣。这项研究揭示了JMJD8与PLIN2之间的物理相互作用，这在驱动脂肪细胞肥大和胰岛素抵抗中起着关键作用。JMJD8通过抑制PLIN2磷酸化来抑制禁食诱导的脂肪自噬并减少能量产生。这些发现突出了JMJD8和PLIN2在调节脂滴稳态中的重要性，并提示了在能量剥夺期间控制脂肪动员的潜在机制。
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