Chronic cold exposure reprograms feeding-regulated LPL activity in white adipose tissues through hepatic ANGPTL3 and ANGPTL8  

作　　者：Yiliang Zhang Shengyang Zhou Runming Zhao Yingzhen Huang Yan Wang 

机构地区：[1]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　　处：《Life Metabolism》2025年第1期57-61,共5页生命代谢(英文)

基　　金：supported by grants from the National Key Research and Development Program of China(2018YFA0800700);the National Natural Science Foundation of China(92057207,32021003,92254308,92357303,323B1015,and 32271223);the 111 Project of China(B16036);the Key Research and Development Program of Hubei province(2019CFA067);Wuhan City(2020020601012211).

摘　　要：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.

关 键 词：LPL WHITE FEEDING 

分 类 号：R589.2[医药卫生—内分泌]