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学科主题基础医学
Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells
Deng, Jingna1,2; Liu, Shangxin1,2; Zou, Liangqiang1,2; Xu, Chong3; Geng, Bin1,2; Xu, Guoheng1,2
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2012-02-24
DOI10.1074/jbc.M111.299115
287期:9页:6240-6249
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]HORMONE-SENSITIVE LIPASE ; PRIMARY RAT ADIPOCYTES ; NECROSIS-FACTOR-ALPHA ; DEPENDENT PROTEIN-KINASE ; LIPID STORAGE DROPLETS ; TRIGLYCERIDE LIPASE ; 3T3-L1 ADIPOCYTES ; STIMULATED LIPOLYSIS ; ER MEMBRANE ; PERILIPIN-A
英文摘要

In obesity and diabetes, adipocytes show significant endoplasmic reticulum (ER) stress, which triggers a series of responses. This study aimed to investigate the lipolysis response to ER stress in rat adipocytes. Thapsigargin, tunicamycin, and brefeldin A, which induce ER stress through different pathways, efficiently activated a time-dependent lipolytic reaction. The lipolytic effect of ER stress occurred with elevated cAMP production and protein kinase A (PKA) activity. Inhibition of PKA reduced PKA phosphosubstrates and attenuated the lipolysis. Although both ERK1/2 and JNK are activated during ER stress, lipolysis is partially suppressed by inhibiting ERK1/2 but not JNK and p38 MAPK and PKC. Thus, ER stress induces lipolysis by activating cAMP/PKA and ERK1/2. In the downstream lipolytic cascade, phosphorylation of lipid droplet-associated protein perilipin was significantly promoted during ER stress but attenuated on PKA inhibition. Furthermore, ER stress stimuli did not alter the levels of hormone-sensitive lipase and adipose triglyceride lipase but caused Ser-563 and Ser-660 phosphorylation of hormone-sensitive lipase and moderately elevated its translocation from the cytosol to lipid droplets. Accompanying these changes, total activity of cellular lipases was promoted to confer the lipolysis. These findings suggest a novel pathway of the lipolysis response to ER stress in adipocytes. This lipolytic activation may be an adaptive response that regulates energy homeostasis but with sustained ER stress challenge could contribute to lipotoxicity, dyslipidemia, and insulin resistance because of persistently accelerated free fatty acid efflux from adipocytes to the bloodstream and other tissues.

语种英语
WOS记录号WOS:000300791800017
项目编号2009CB941603 ; 2012CB517505 ; 81070114 ; 30890042
资助机构National Basic Research Program of China ; National Natural Science Foundation of China
引用统计
被引频次:48[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52863
专题北京大学基础医学院
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Astronaut Res & Training Ctr China, Beijing 100094, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
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GB/T 7714
Deng, Jingna,Liu, Shangxin,Zou, Liangqiang,et al. Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2012,287(9):6240-6249.
APA Deng, Jingna,Liu, Shangxin,Zou, Liangqiang,Xu, Chong,Geng, Bin,&Xu, Guoheng.(2012).Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells.JOURNAL OF BIOLOGICAL CHEMISTRY,287(9),6240-6249.
MLA Deng, Jingna,et al."Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells".JOURNAL OF BIOLOGICAL CHEMISTRY 287.9(2012):6240-6249.
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