초록 close

본 연구는 지구성 운동에 의한 glucose transporter(GLUT)4의 생합성에 myocyte enhance factor(MEF)2C가 어떠한 역할을 수행하는지 확인하는 것이다. GLUT4 발현에 대한 MEF2A와 MEF2C의 역할을 확인하기 위하여 MEF2A와 MEF2C를 생쥐의 골격근 세포에 과발현 시켰다. 2주간 수영 운동을 실시한 흰쥐의 삼두근을 적출하여 GLUT 생합성에 관련된 인자를 분석하였다. MEF2C 발현에 대한 PPARβ/δ의 역할을 확인하기 위해 전기 유전자 전이법을 이용하여 생쥐의 tibialis anterior(TA) 근육과 흰쥐의 epitrochlearis 근육에 각각 PPARβ/δ와 shPPARβ/δ의 과발현을 유도하였다. MEF2A 또는 MEF2C가 과발현 된 근세포에서 GLUT4의 발현이 empty vector(EV)를 처치한 세포보다 각각 2.8배와 2.5배 증가하였다. 2주간 수영 운동을 실시한 흰쥐의 골격근에서 PPARβ/δ, peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC-1α), GLUT4 그리고 MEF2A의 발현이 좌업 그룹보다 각각 2.2, 2.7, 2.3 그리고 2.5배 증가하였으나, MEF2C는 차이가 없는 것으로 나타났다. PPARβ/δ가 과발현 된 골격근에서 MEF2A와 GLUT4는 EV 처치된 근육보다 각각 1.9배와 2.1배 증가하였으나, MEF2C는 55% 감소하였다. shPPARβ/δ가 과발현 된 골격근에서 MEF2A는 scramble(Scr) 처치된 근육보다 61% 감소하였으나, MEF2C는 1.8배 증가하였다. 따라서 지구성 운동에 의한 GLUT4의 생합성은 MEF2A에 의하여 조절되며, PGC-1α에 의한 MEF2C-GLUT4 생합성 기전은 PPARβ/δ에 의하여 상쇄된다.


The purpose of this study was to identify the role of MEF2C on GLUT4 following endurance exercise, peroxisome proliferator-activated receptor beta/delta(PPARβ/δ) and shPPARβ/δ over-expression. To evaluate the role of MEF2A and MEF2C on GLUT4 expression, MEF2A and MEF2C was over-expressed in mice skeletal muscle cell(C2C12). Rat triceps muscles were dissected at 18h after 2weeks swimming exercise. To evaluate the role of PPARβ/δ on MEF2C expression, PPARβ/δ was over-expressed in mouse tibialis anterior(TA) muscle and shPPARβ/δ was over-expressed in rat epitrochlearis muscle using electrical pulse-mediated gen transfer(electroporation; EPO) method. GLUT4 in MEF2A and MEF2C over-expressed C2C12 were increased 2.8 and 2.5 fold respectively when compared to an empty vector(EV) treated group. PPARβ/δ, PGC-1α, GLUT4 and MEF2A in swimming exercise skeletal muscle for 2 weeks were increased 2.2, 2.7, 2.3 and 2.5 fold respectively than sedentary(Sed) skeletal muscle, but MEF2C in swimming exercise skeletal muscle for 2 weeks were not increased than Sed skeletal muscle. MEF2A and GLUT4 in PPARβ/δ over-expressed skeletal muscle by EPO were increased 1.9 and 2.1 fold respectively when compared to an EV treated skeletal muscle, but MEF2C in PPARβ/δ over-expressed skeletal muscle by EPO were decreased 55% when compared to an EV treated skeletal muscle. MEF2A in shPPARβ/δ over-expressed skeletal muscle by EPO were decreased 61% when compared to a scramble(Scr) treated skeletal muscle. MEF2C in shPPARβ/δ over-expressed skeletal muscle by EPO were increased 1.8 fold when compared to a scramble(Scr) treated skeletal muscle. Our results indicate that GLUT4 biogenesis following endurance exercise is controlled by MEF2A, PPARβ/δ countervail PGC-1α effect on GLUT4 biogenesis by MEF2C.