Triglyceride Synthesis by DGAT1 Protects Adipocytes from Lipid-Induced ER Stress during Lipolysis.
Triglyceride Synthesis by DGAT1 Protects Adipocytes from Lipid-Induced ER Stress during Lipolysis.
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DOI：
10.1016/j.cmet.2017.07.012
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发表时间：
2017-08-01
期刊：
影响因子：
29
通讯作者：
Farese RV Jr
中科院分区：
文献类型：
--
作者：
Chitraju C;Mejhert N;Haas JT;Diaz-Ramirez LG;Grueter CA;Imbriglio JE;Pinto S;Koliwad SK;Walther TC;Farese RV Jr
Triglyceride (TG) storage in adipose tissue provides the major reservoir for metabolic energy in mammals. During lipolysis, fatty acids (FAs) are hydrolyzed from adipocyte TG stores and transported to other tissues for fuel. For unclear reasons, a large portion of hydrolyzed FAs in adipocytes is re-esterified to TGs in a “futile”, ATP-consuming, energy dissipating cycle. Here we show that FA re-esterification during adipocyte lipolysis is mediated by DGAT1, an ER-localized DGAT enzyme. Surprisingly, this re-esterification cycle does not preserve TG mass, but instead functions to protect the ER from lipotoxic stress and related consequences, such as adipose tissue inflammation. Our data reveal an important role for DGAT activity and TG synthesis generally in averting ER stress and lipotoxicity, with specifically DGAT1 performing this function during stimulated lipolysis in adipocytes. Chitraju et al. unravel a 60+-year old mystery of why a large portion of hydrolyzed FAs in adipocytes is re-esterified to TGs during lipolysis. They show show the ER enzyme DGAT1 mediates this FA re-esterification, not preserve TG mass, but instead to protect the ER from lipotoxicity.
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