Transgenic UCP1 in white adipocytes modulates mitochondrial membrane potential

FEBS Letters

Horáková, Milada¹  Floryk, Daniel¹  Kopecký, Jan¹  Baumruk, Filip¹  Flachs, Pavel¹ 

[1] Institute of Physiology, Academy Sciences of the Czech Republic, Vı́deňská 1083, 142 20 Prague, Czech Republic

关键词: Oxidative phosphorylation;    Energy metabolism;    Proton leak;    Flow cytometry;    Tetramethylrhodamine methyl ester;    UCP;    uncoupling protein;    aP2-Ucp mice;    transgenic mice with synthesis of UCP1 from adipocyte lipid binding protein promoter;    IFL;    mean fluorescence;    TMRM;    tetramethylrhodamine methyl ester;    BSA;    bovine serum albumin;    FCCP;    carbonylcyanide p-trifluoromethoxyphenylhydrazone;    ΔΨ m;    mitochondrial membrane potential;    KCl buffer;    100 mM KCl;    10 mM Tris;    2 mM MgCl2;    4 mM K2HPO4 and 1 mM EDTA;   

DOI  :  10.1016/S0014-5793(99)00053-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

To test if mitochondrial uncoupling in white adipocytes is responsible for obesity resistance of the aP2-Ucp transgenic mice expressing ectopic uncoupling protein 1 (UCP1) in white fat, mitochondrial membrane potential (ΔΨ _m) was estimated by flow cytometry in adipocytes isolated from gonadal fat. Ectopic UCP1 (approximately 0.8 mol UCP1/mol respiratory chain) decreased the ΔΨ _m and rendered the potential sensitive to GDP and fatty acids. These ligands of UCP1 had no effect on ΔΨ _m in white adipocytes from non-transgenic mice, suggesting that the function of endogenous UCP2 in adipocytes was not affected. The results support the hypothesis that mitochondrial uncoupling in white fat may prevent development of obesity.

【 授权许可】

Unknown