일회성 저강도 지구성운동 시 MEF2A를 통한 PPARδ의 GLUT4 생합성 조절 = Control of GLUT4 biogenesis through PPARδ and MEF2A axis with single bout of low-intensity endurance exercise in rodent skeletal muscle

다국어 초록 (Multilingual Abstract)

PURPOSE: There is increasing evidence that the regulator of skeletal muscle metabolism, PPARδ is associated with GLUT4 biogenesis. But, whether acute low-intensity endurance exercise affects PPARδ and the mechanism of GLUT4 biogenesis has not been clearly identified. Even Though GLUT4 expression is increased by acute low-intensity endurance exercise. PPARδ expression by acute low-intensity endurance exercise is unclear. PPARδ was shown to induce the expression of PGC-1α in skeletal muscle. Since both are increased with acute low-intensity endurance exercise, it is difficult to determine whether one or both, induce GLUT4 biogenesis in skeletal muscle. METHODS: This study measured PPARδ expression in skeletal muscle by acute low-intensity endurance exercise and confirmed the effect of PPARδ on GLUT4 biogenesis in PGC-1α KO mice. Sixteen rats were randomly assigned into 2 groups(Sedentary, Sed & 1 day exercise, 1d Ex). Exercise groups performed a 6 hours low-intensity swimming program. RESULTS: The expressions of GLUT4, PGC-1α and PPARδ were increased in the 1d Ex group from the Sed group. PPARδ was overexpressed using electric pulse-mediated gene transfer technique in PGC-1α KO mice to confirm effects of PPARδ for GLUT4 biogenesis without PGC-1α. The expressions of GLUT4 and MEF2A were increased in PPARδ overexpressed muscles. CONCLUSIONS: These findings suggest that PPARδ-driven GLUT4 biogenesis through MEF2A by acute low-intensity endurance exercise was independent of PGC-1α.