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자료유형
학술저널
저자정보
저널정보
한국운동생리학회 운동과학 운동과학 제24권 제3호
발행연도
2015.1
수록면
289 - 295 (7page)

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PURPOSE: The aim of this study was to identified which PPARβ/δ control PGC-1α protein stability in rat skeletal muscle by long-term endurance exercise. METHODS: shPPARβ/δ was over-expressed in rat epitrochlearis (Epi) muscle using electrical pulse-mediated gen transfer (electroporation; EPO) method. Then animal underwent 2 wk long swimming exercise. To evaluate PPARβ/δ, PGC-1α ubiquitination, PGC-1α and mitochondrial enzyme expression in rat skeletal muscle, Epi muscles were dissected 18h post final bout of swimming exercise. RESULTS: PPARβ/δ, PGC-1α, COX I and NADH protein expression in shPPARβ/δ over-expression sedentary (Sed) skeletal muscle were significantly decreased over 55%, but PGC-1α ubiquitination was significantly increased 2.6 fold when compared to scramble (Scr) treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with Scr gene treated muscle were significantly increased over 2 fold, but PGC-1α ubiquitination was significantly decreased 66% when compared to Scr gene treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with shPPARβ/δ gene treated muscle were not increased, but PGC-1α ubiquitination was significantly increased 1.96 fold when compared to Scr gene treated Sed muscle. CONCLUSIONS: Our results indicate that PPARβ/δ controls PGC-1α protein stability in rat skeletal muscle following long-term endurance exercise.

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