You Dongjoo, Kang Sona
Nutritional Sciences and Toxicology Department, University of California, Berkeley, Berkeley, CA.
Diabetes. 2025 Apr 1;74(4):458-471. doi: 10.2337/db23-0883.
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.
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。
