Ozaki N, Sato E, Kurokawa T, Ishibashi S
Department of Physiological Chemistry, Hiroshima University School of Medicine, Japan.
Mech Ageing Dev. 1996 Jul 17;88(3):149-58. doi: 10.1016/0047-6374(96)01733-2.
The content of facilitative glucose transporter proteins in the heart, lung, liver, testis and cerebellum of SAMP8, a substrain of senescence-accelerated prone mouse, was investigated. The increase in the expression of facilitative glucose transporter proteins, estimated by the D-glucose inhibitable cytochalasin B binding assay, was observed only in the heart of 4-8 week old SAMP8 in comparison with SAMR1, a substrain of senescence-accelerated resistant mouse. The increase in cytochalasin B binding protein in SAMP8 was restricted at 4-8 weeks old, thereafter no significant difference was observed between the two substrains. Furthermore, the immunoblotting revealed that the content of the GLUT4 (glucose transporter isoform 4) protein in the crude membranes prepared from 4-8 week old SAMP8 was greater than that of SAMR1, without the difference in the content of the GLUT1 (glucose transporter isoform 1) protein. Additionally, the increased GLUT4 protein in SAMP8 was localized in the intracellular membranes. These results suggest that an accelerated ageing of SAMP8 is possibly related to the overproduction of the energy in the heart through the increase in glucose uptake after the translocation of GLUT4 from the intracellular pools to the plasma membranes.
研究了衰老加速易感性小鼠亚系SAMP8的心脏、肺、肝脏、睾丸和小脑中促进性葡萄糖转运蛋白的含量。通过D - 葡萄糖抑制的细胞松弛素B结合试验估计,与衰老加速抗性小鼠亚系SAMR1相比,仅在4 - 8周龄SAMP8的心脏中观察到促进性葡萄糖转运蛋白表达增加。SAMP8中细胞松弛素B结合蛋白的增加在4 - 8周龄时受到限制,此后两个亚系之间未观察到显著差异。此外,免疫印迹显示,从4 - 8周龄SAMP8制备的粗膜中GLUT4(葡萄糖转运异构体4)蛋白的含量高于SAMR1,而GLUT1(葡萄糖转运异构体1)蛋白的含量没有差异。此外,SAMP8中增加的GLUT4蛋白定位于细胞内膜。这些结果表明,SAMP8的加速衰老可能与GLUT4从细胞内池转运到质膜后葡萄糖摄取增加导致心脏能量过度产生有关。