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  • Title: Voluntary running improves in vivo insulin resistance in high-salt diet fed rats.
    Author: Qin B, Oshida Y, Li P, Kubota M, Nagasaki M, Sato Y.
    Journal: Exp Biol Med (Maywood); 2007 Nov; 232(10):1330-7. PubMed ID: 17959846.
    Abstract:
    It is well known that exercise training, including voluntary running (VR), improves insulin resistance. However, the effect of VR on insulin resistance induced by high salt intake is unclear. The aim of this study was to determine whether VR would improve the glucose utilization in normal male Sprague-Dawley rats fed a high-salt diet (HSD) on 2-week early prevention and 1-week midway intervention protocols. In vivo glucose utilization was measured by euglycemic clamp technique. Further analyses of the possible changes in insulin signaling occurring in skeletal muscle were performed by Western blot and reverse transcription polymerase chain reaction (RT-PCR). The glucose infusion rates (GIRs) after 2 weeks of HSD feeding were decreased (HSD vs. control: 21.5 +/- 0.8 vs. 27 +/- 0.5 mg/kg body wt/min; P < 0.05), and improved by 2 weeks VR to 30.5 +/- 1.5 mg/kg body wt/min. Additionally, the GIRs after 3 weeks of HSD feeding were decreased (HSD vs. control: 20.0 +/- 0.3 vs. 26.5 +/- 0.6 mg/kg body wt/min; P < 0.05), and they also improved by the third week of VR (28.5 +/- 0.7 mg/ kg body wt/min vs. sedentary; P < 0.01). There were no differences in skeletal muscle for the total mass of insulin receptor-beta (IR-beta), IR substrate-1 (IRS-1), Akt, and glucose transporter 4 (GLUT4) in any of the groups of 2 weeks of HSD loading control and VR. VR did not regulate the enhanced tyrosine phosphorylation of IR-beta and IRS-1 by 2 weeks of HSD feeding. However, the enhanced serine phosphorylation of Akt and the tyrosine phosphorylation of GLUT4 were significantly inhibited by the early VR. HSD also impaired GLUT4 content in the plasma membrane and mRNA expression, but the decreases were improved by 2 weeks of VR. These results suggest that early voluntary exercise would prevent the development of insulin resistance induced by an HSD due in part by enhancing the impaired GLUT4 translocation and mRNA expression in skeletal muscle.
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