Azoxystrobin, a mitochondrial complex III Q(o) site inhibitor, exerts beneficial metabolic effects in vivo and in vitro
文献类型：期刊论文
| 作者 | Gao, An-Hui1,2; Fu, Yan-Yun2; Zhang, Kun-Zhi1; Zhang, Mei2 ; Jiang, Hao-Wen1; Fan, Li-Xia1; Nan, Fa-Jun2; Yuan, Chong-Gang1; Li, Jia1,2; Zhou, Yu-Bo2
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| 刊名 | BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
 |
| 出版日期 | 2014-07 |
| 卷号 | 1840期号:7页码:2212-2221 |
| 关键词 | Azoxystrobin Mitochondria complex III Metabolic diseases AMP-activated protein kinase |
| ISSN号 | 0304-4165 |
| DOI | 10.1016/j.bbagen.2014.04.002 |
| 文献子类 | Article |
| 英文摘要 | Background: Several anti-diabetes drugs exert beneficial effects against metabolic syndrome by inhibiting mitochondrial function. Although much progress has been made toward understanding the role of mitochondrial function inhibitors in treating metabolic diseases, the potential effects of these inhibitors on mitochondrial respiratory chain complex III remain unclear. Methods: We investigated the metabolic effects of azoxystrobin (AZOX), a Q(o) inhibitor of complex III, in a high-fat diet-fed mouse model with insulin resistance in order to elucidate the mechanism by which AZOX improves glucose and lipid metabolism at the metabolic cellular level. Results: Acute administration of AZOX in mice increased the respiratory exchange ratio. Chronic treatment with AZOX reduced body weight and significantly improved glucose tolerance and insulin sensitivity in high-fat diet-mice. AZOX treatment resulted in decreased triacylglycerol accumulation and down-regulated the expression of genes involved in liver lipogenesis. AZOX increased glucose uptake in L6 myotubes and 3T3-L1 adipocytes and inhibited de novo lipogenesis in HepG2 cells. The findings indicate that AZOX-mediated alterations to lipid and glucose metabolism may depend on AMP-activated protein kinase (AMPK) signaling. Conclusions: AZOX, a Q(o) inhibitor of mitochondrial respiratory complex III, exerts whole-body beneficial effects on the regulation of glucose and lipid homeostasis in high-fat diet-fed mice. General significance: These findings provide evidence that a Q(o) inhibitor of mitochondrial respiratory complex III could represent a novel approach for the treatment of obesity. (C) 2014 Elsevier B.V. All rights reserved. |
| WOS关键词 | ACTIVATED PROTEIN-KINASE ; MUSCLE INSULIN-RESISTANCE ; STIMULATED GLUCOSE-UPTAKE ; CYTOCHROME BC(1) COMPLEX ; FATTY-ACID OXIDATION ; SKELETAL-MUSCLE ; RESPIRATORY-CHAIN ; AMP ; MECHANISM ; OBESITY |
| 资助项目 | National Program on Key Basic Research Project 973 Program[2012CB524906] ; National Science and Technology Major Projects for "Major New Drugs Innovation and Development"[2012ZX09301001-004] ; National Natural Science Foundation of China[81125023] ; National Natural Science Foundation of China[81270942] ; National Natural Science Foundation of China[81001463] |
| WOS研究方向 | Biochemistry & Molecular Biology ; Biophysics |
| 语种 | 英语 |
| WOS记录号 | WOS:000338402400012 |
| 出版者 | ELSEVIER SCIENCE BV |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/277009]  |
| 专题 | 国家新药筛选中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Yuan, Chong-Gang |
| 作者单位 | 1.E China Normal Univ, Sch Life Sci, Physiol Lab, Shanghai 200062, Peoples R China; 2.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Natl Ctr Drug Screening, Shanghai 200031, Peoples R China |
| 推荐引用方式 GB/T 7714 | Gao, An-Hui,Fu, Yan-Yun,Zhang, Kun-Zhi,et al. Azoxystrobin, a mitochondrial complex III Q(o) site inhibitor, exerts beneficial metabolic effects in vivo and in vitro[J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,2014,1840(7):2212-2221. |
| APA | Gao, An-Hui.,Fu, Yan-Yun.,Zhang, Kun-Zhi.,Zhang, Mei.,Jiang, Hao-Wen.,...&Li, Jing-Ya.(2014).Azoxystrobin, a mitochondrial complex III Q(o) site inhibitor, exerts beneficial metabolic effects in vivo and in vitro.BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,1840(7),2212-2221. |
| MLA | Gao, An-Hui,et al."Azoxystrobin, a mitochondrial complex III Q(o) site inhibitor, exerts beneficial metabolic effects in vivo and in vitro".BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS 1840.7(2014):2212-2221. |
入库方式： OAI收割
来源：上海药物研究所
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