慢性冷暴露通过肝脏ANGPTL3和ANGPTL8重新编程摄食调节的白色脂肪组织中的LPL活性。

Life metabolism Pub Date : 2024-10-16 eCollection Date: 2025-02-01 DOI:10.1093/lifemeta/loae037
Yiliang Zhang, Shengyang Zhou, Runming Zhao, Yingzhen Huang, Yan Wang
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引用次数: 0

摘要

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ANGPTL3 (A3)和ANGPTL8 (A8)形成复合物,通过体循环抑制白色脂肪组织(WAT)中的LPL活性。ANGPTL4 (A4)在WAT中表达,局部抑制LPL活性。摄食增加肝脏A8表达,与A3一起增强其对WAT LPL活性的抑制作用,而摄食抑制WAT A4表达,释放其对LPL的抑制作用。在室温下,摄食抑制的A4覆盖了摄食增加的A3/A8,导致食物摄入导致WAT中LPL活性增加。褐变可改善肝脏胰岛素敏感性,增加餐后A8表达。摄食增加的A3/A8覆盖了摄食抑制的A4,导致WAT中LPL活性受到食物摄入的抑制。这种重编程的LPL调节在脂肪组织褐变过程中重编程TG代谢中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic cold exposure reprograms feeding-regulated LPL activity in white adipose tissues through hepatic ANGPTL3 and ANGPTL8.

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.

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