长期冷暴露通过肝脏血管生成素样蛋白3（ANGPTL3）和血管生成素样蛋白8（ANGPTL8）重新编程白色脂肪组织中进食调节的脂蛋白脂肪酶（LPL）活性。
Chronic cold exposure reprograms feeding-regulated LPL activity in white adipose tissues through hepatic ANGPTL3 and ANGPTL8.
作者信息
Zhang Yiliang, Zhou Shengyang, Zhao Runming, Huang Yingzhen, Wang Yan
机构信息
Hubei Key Laboratory of Cell Homeostasis, Department of Biochemistry, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, Hubei 430072, China.
出版信息
Life Metab. 2024 Oct 16;4(1):loae037. doi: 10.1093/lifemeta/loae037. eCollection 2025 Feb.
Graphical Abstract Lipoprotein lipase (LPL) mediates peripheral tissue triglyceride (TG) uptake. Hepatic ANGPTL3 (A3) and ANGPTL8 (A8) form a complex and inhibit LPL activity in the white adipose tissue (WAT) via systematic circulation. ANGPTL4 (A4) is expressed in WAT and inhibits LPL activity locally. Feeding increases hepatic A8 expression and increases its inhibition for WAT LPL activity together with A3, while feeding suppresses WAT A4 expression and releases its inhibition on LPL. At room temperature, the feeding-suppressed A4 overrides the feeding-increased A3/A8, resulting in increased LPL activity in WAT by food intake. Browning improves hepatic insulin sensitivity and increases postprandial A8 expression. The feeding-increased A3/A8 overrides the feeding-suppressed A4, resulting in suppressed LPL activity in WAT by food intake. This reprogrammed LPL regulation plays an important role in reprogramming TG metabolism during adipose tissue browning.
图形摘要
脂蛋白脂肪酶（LPL）介导外周组织甘油三酯（TG）摄取。肝脏血管生成素样蛋白3（ANGPTL3，A3）和血管生成素样蛋白8（ANGPTL8，A8）形成复合物，并通过体循环抑制白色脂肪组织（WAT）中的LPL活性。血管生成素样蛋白4（ANGPTL4，A4）在WAT中表达并局部抑制LPL活性。进食会增加肝脏A8表达，并与A3一起增强其对WAT中LPL活性的抑制作用，而进食会抑制WAT中A4表达并解除其对LPL的抑制。在室温下，进食抑制的A4会超过进食增加的A3/A8，导致进食使WAT中的LPL活性增加。褐色变可改善肝脏胰岛素敏感性并增加餐后A8表达。进食增加的A3/A8会超过进食抑制的A4，导致进食使WAT中的LPL活性受到抑制。这种重新编程的LPL调节在脂肪组织褐色变过程中对TG代谢的重新编程中起重要作用。
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