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NTIS 바로가기생명과학회지 = Journal of life science, v.19 no.5 = no.109, 2009년, pp.644 - 651
배희숙 (한국체육대학교 체육과학관 운동생화학실) , 엄현섭 (한국체육대학교 체육과학관 운동생화학실) , 강은범 (한국체육대학교 체육과학관 운동생화학실) , 양춘열 (한국체육대학교 체육과학관 운동생화학실) , 이용로 (한국체육대학교 체육과학관 운동생화학실) , 이창국 (순천향대학교 체육학과) , 천우호 (순천향대학교 체육학과) , 전혜자 (순천향대학교 체육학과) , 조인호 (한국체육대학교 체육과학관 운동생화학실) , 조준용 (한국체육대학교 체육과학관 운동생화학실)
The objective of this study was to identify EXE (1 hr a day at 21 m/min for 5 day/wk, at 0 % grade for 6 wk) on myocardium glucose metabolic phenotypic proteins (AMPK-PGC-1
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핵심어 | 질문 | 논문에서 추출한 답변 |
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지구성 운동이 당뇨 조건에서 심근의 당 대사를 개선하고 심장을 보호하는 데 효과가 있는지를 검증한 결과는 무엇인가? | 그 결과 STZ-IRI의 경우 전형적인 당뇨의 특성인 고혈당 증세와 함께 심장의 생리적 지표인 좌심실내압이 현저하게 낮은 것으로 나타났으며 대부분 동물조직에 존재하며 에너지원-감지 효소(fuel-sensing enzyme)로서 심근과 골격근에서 지방산 산화와 포도당 흡수를 촉진시키는데 관여하는 AMPK, 대사적 조절인자로서 포도당과 지질 산화에 관여하는 PGC-1 α, 심근세포내로 포도당 운반 역할을 하는 포도당 수송체인 GLUT-4와 단백질 구조 변형을 억제하고 조직을 보호하는 단백질인 HSP-60 발현량이 허혈 처치 운동집단에 비해 현저하 게 낮은 것으로 나타났다. 이러한 결과는 당뇨 조건하에서 인슐린 결핍, 고혈당과 심장의 좌심실내압과 AMPK, PGC-1α, GLUT-4와 HSP-60 발현량 감소는 심장 기능이상, 심근의 포도당과 대사 이상뿐만 아니라 병리학적 심근비대를 유발시킨다고 제시한 Li 등[25], Sriwijitkamol 등[48], Chen 등[7], Garvey 등[15], Liao 등[27], Patti 등[36]과 Shan 등[45]의 결과와 일치 하는 것으로 나타났다. | |
허혈에 의한 심근의 손상은 어떤 것을 유도하는가? | 심혈관질환들 중 관상동맥질환의 병리학적 증후는 허혈 (ischemia)에 의한 심근 손상으로 보고되고 있다[43]. 허혈에 의한 심근의 손상은 심장 기능의 저하로 인한 심근 세포 사멸을 유도하며[40] 특히 당뇨병성 심장은 허혈 손상에 가장 민감하게 반응하는 것으로 당뇨 질환 모델의 동물 실험을 통하여 보고되고 있다[11,42]. 이러한 당뇨 성 심장질환 개선을 위한 방법으로 심장의 허혈성 전 처치(ischemic preconditioning)에 의한 심근보호 효과에 대해 여러 학자들이 관심을 갖고 연구들을 수행해왔다. | |
당뇨병은 어떻게 당뇨환자의 사망률을 증가시키는가? | 당뇨병은 산화적 스트레스로 인한 세포내 방어 시스템 손상을 초래하여 세포사멸을 가속화시켜 심근경색으로 인한 당뇨환자들의 사망률을 증가시킨다[2,11,42]. 특히, 당뇨병은 심근 세포내 단백질의 3차 구조를 유지시켜 세포손상을 최소화 하고 항상성 유지에 중요한 역할을 하는 분자 샤페론의 일종인 열충격 단백질(heat shock proteins)합성의 감소와 당대사 관련 단백질인 AMPK (AMP-activated protein kinase), PGC-1α (peroxisome proliferator activated receptor coactivator-1α)와 GLUT-4 (glucose transporter-4)의 발현량을 감소시켜 심근의 세포손상과 당 대사 저하를 유발시킨다[14, 19,25,27,36,41,48,49,51]. |
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