IR@PKUHSC  > 北京大学基础医学院
学科主题基础医学
Increase or Decrease Hydrogen Sulfide Exert Opposite Lipolysis, but Reduce Global Insulin Resistance in High Fatty Diet Induced Obese Mice
Geng, Bin1; Cai, Bo1,2; Liao, Feng1; Zheng, Yang1; Zeng, Qiang3; Fan, Xiaofang4; Gong, Yongsheng4; Yang, Jichun1; Cui, Qing Hua1; Tang, Chaoshu1,4; Xu, Guo Heng1
刊名PLOS ONE
2013-09-13
DOI10.1371/journal.pone.0073892
8期:9
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]HORMONE-SENSITIVE LIPASE ; ADIPOSE TRIGLYCERIDE LIPASE ; GAMMA-GLUTAMYL-TRANSFERASE ; PROTEIN-KINASE ; GLUCOSE-UTILIZATION ; 3T3L1 ADIPOCYTES ; PLASMA CYSTEINE ; METABOLISM ; PHOSPHORYLATION ; ACTIVATION
英文摘要

Objective: Adipose tissue expressed endogenous cystathionine gamma lyase (CSE)/hydrogen sulfide (H2S) system. H2S precursor inhibited catecholamine stimulated lipolysis. Thus, we hypothesized that CSE/H2S system regulates lipolysis which contributed to the pathogenesis of insulin resistance.

Methods: We treated rat adipocyte with DL-propargylglycine (PAG, a CSE inhibitor), L-cysteine (an H2S precursor) plus pyridoxial phosphate (co-enzyme) or the H2S chronic release donor GYY4137, then the glycerol level was assayed for assessing the lipolysis. Then, the effects of PAG and GYY4137 on insulin resistance in high fatty diet (HFD) induced obese mice were investigated.

Results: Here, we found that PAG time-dependently increased basal or isoproterenol stimulated lipolysis. However, L-cysteine plus pyridoxial phosphate or GYY4137 significantly reduced it. PAG increased phosphorylated protein kinase A substrate, perilipin 1 and hormone sensitive lipase, but L-cysteine and GYY4137 decreased the parameters. In HFD induced obese mice, PAG increased adipose basal lipolysis, thus blunted fat mass increase, resulting in lowering insulin resistance evidenced by reduction of fasting glucose, insulin level, HOMA index, oral glucose tolerance test (OGTT) curve area and elevating the insulin tolerance test (ITT) response. GYY4137 inhibited lipolysis in vivo without increasing fat mass, but also ameliorated the insulin resistance in HFD mice.

Conclusion: These results implicated that inhibition endogenous CSE/H2S system in adipocytes increased lipolysis by a protein kinase A-perilipin/hormone-sensitive lipase pathway, thus blunted fat mass increase and reduced insulin resistance in obese mice; giving H2S donor decreased lipolysis, also reduced insulin resistance induced by HFD. Our data showed that increase or decrease H2S induced opposite lipolysis, but had the same effect on insulin resistance. The paradoxical regulation may be resulted from different action of H2S on metabolic and endocrine function in adipocyte.

语种英语
WOS记录号WOS:000324408400039
项目编号2012CB517806 ; 2009CB941603 ; 81170235 ; 81070114
资助机构Major State Basic Research Development Program of the People&prime ; s Republic of China ; National Natural Science Foundation of the People&prime ; s Republic China
引用统计
被引频次:23[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/400002259/50425
专题北京大学基础医学院
作者单位1.Guangdong Med Collage, Dept Physiol, Zhan Jiang, Guangdong, Peoples R China
2.Peking Univ, Dept Physiol & Pathophysiol, Sch Basic Med Sci, Beijing 100871, Peoples R China
3.Chinese Peoples Liberat Army Gen Hosp, Int Med Ctr, Beijing, Peoples R China
4.Wenzhou Med Univ, Inst Hypoxia Med, Wen Zhou, Zhejiang, Peoples R China
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GB/T 7714
Geng, Bin,Cai, Bo,Liao, Feng,et al. Increase or Decrease Hydrogen Sulfide Exert Opposite Lipolysis, but Reduce Global Insulin Resistance in High Fatty Diet Induced Obese Mice[J]. PLOS ONE,2013,8(9).
APA Geng, Bin.,Cai, Bo.,Liao, Feng.,Zheng, Yang.,Zeng, Qiang.,...&Xu, Guo Heng.(2013).Increase or Decrease Hydrogen Sulfide Exert Opposite Lipolysis, but Reduce Global Insulin Resistance in High Fatty Diet Induced Obese Mice.PLOS ONE,8(9).
MLA Geng, Bin,et al."Increase or Decrease Hydrogen Sulfide Exert Opposite Lipolysis, but Reduce Global Insulin Resistance in High Fatty Diet Induced Obese Mice".PLOS ONE 8.9(2013).
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