| 지구성 운동에 의하여 증가된 PPARβ/δ는 NRF-1 promoter 활성을 통하여 생쥐 근육내 GLUT4 및 미토콘드리아 효소의 발현을 유도한다 |
| 고진호1, 김기진2, 정수련3, 김상현2 |
1Washington university school of medicine
2계명대학교
3경주대학교 |
| The increased PPARβ/δ by endurance exercise control MEF2A-GLUT4 and mitochodrial enzymes through NRF-1 promoter activity in mouse skeletal muscle |
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| ABSTRACT |
PURPOSE:
The propose of this study was to evaluate whether PPARβ/δ can increase mitochondrial enzymes and GLUT4 through NRF-1 promoter activity.
METHODS:
To evaluate, PPARβ/δ and NRF-1 protein expression in mouse skeletal muscle, TA muscle were dissect at 24h after 10 day swimming exercise(Ex). To evaluate PPARβ/δ effects on gene regulation, PPARβ/δ was overexpressed in mouse TA muscle using electrical pulse-mediated gen transfer(electroporation; EPO) method. We conducted chip and promoter reporter assay to confirm of PPARβ/δ can bind NRF-1 promoter and activates NRF-1 promoter in mouse muscle cell.
RESULTS:
PPARβ/δ and NRF-1 protein expression in skeletal muscle of 10 day Ex group were increased 2.2 and 2.7 fold respectively when compare to non-exercise muscle. PGC-1α protein expression in PPARβ/δ overexpression skeletal muscle were not different, but NRF-1, MEF2A, GLUT4, ATP syn and Cyt C expression were increased 2.2, 2.3, 2.1, 2 and 1.7 fold respectively when compare to empty vector(EV) treated muscle. Our ChiP and promoter activity assay result show that NRF-1 promoter has a PPARβ/δ binding site(PPRE) and PPARβ/δ can activates NRF-1 promoter through the PPRE.
CONCLUSIONS:
The increased PPARβ/δ by endurance exercise can control MEF2A-GLUT4 and mitochodrial enzymes such as ATP syn and Cyt C through NRF-1 promoter activity. |
| Key words:
Endurance exercise, PPARβ/δ, NRF-1, GLUT4, mitochondrial enzymes |
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