Abstract

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.

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