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    지구성 운동과 인슐린 복합처치가 심장과 폐의 Akt 인산화에 미치는 영향 = The effect of endurance exercise and insulin on Akt phosphorylation in mouse heart and Lung

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    https://www.riss.kr/link?id=A75521126

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Endurance exercise and insulin play a key role in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of insulin receptor (IR). Akt is known to play an critical role in promoting cell survival, inhibiting cell apoptosis, and enhancing glucose uptake and transport. Even though exercise increases glucose transport and glycogen synthesis as insulin does, the relationship of exercise and Akt is not elucidated yet. To determine whether exercise or/and insulin activate Akt in mouse heart and lung, C57BL/6J male mice were divided into four groups (C; control group, E; endurance exercise group, I; insulin treat group, and E+I; endurance exercise and insulin group). Though, Akts in heart and lung were not phosphorylated in E (17 m/min, 10%), Akt in heart and lung was phosphorylated significantly in E+I and I (2.5 unit). Especially, lung Akt phosphorylation in E+I was increased significantly compared with that of I (4.9±0.2 vs 4.0±0.1, p<.05). Furthermore, the lung IR phosphorylation in E+I was increase significantly more than that of I (5.9±0.4 vs 4.5±0.3, p<.05). The increase of lung Akt phosphorylation in E+I was thought to be followed by IR phosphorylation. In conclusion, one hour endurance exercise enhances IR phosphorylation induced by insulin in mouse lung. This increased IR phosphorylation by endurance exercise may enhance insulin-induced Akt phosphorylation.
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    Endurance exercise and insulin play a key role in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of insulin receptor (IR). Akt is known to play an critical role in promoting cell sur...

    Endurance exercise and insulin play a key role in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of insulin receptor (IR). Akt is known to play an critical role in promoting cell survival, inhibiting cell apoptosis, and enhancing glucose uptake and transport. Even though exercise increases glucose transport and glycogen synthesis as insulin does, the relationship of exercise and Akt is not elucidated yet. To determine whether exercise or/and insulin activate Akt in mouse heart and lung, C57BL/6J male mice were divided into four groups (C; control group, E; endurance exercise group, I; insulin treat group, and E+I; endurance exercise and insulin group). Though, Akts in heart and lung were not phosphorylated in E (17 m/min, 10%), Akt in heart and lung was phosphorylated significantly in E+I and I (2.5 unit). Especially, lung Akt phosphorylation in E+I was increased significantly compared with that of I (4.9±0.2 vs 4.0±0.1, p<.05). Furthermore, the lung IR phosphorylation in E+I was increase significantly more than that of I (5.9±0.4 vs 4.5±0.3, p<.05). The increase of lung Akt phosphorylation in E+I was thought to be followed by IR phosphorylation. In conclusion, one hour endurance exercise enhances IR phosphorylation induced by insulin in mouse lung. This increased IR phosphorylation by endurance exercise may enhance insulin-induced Akt phosphorylation.

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    공동연구자 (7)

    유사연구자 (20) 활용도상위20명

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    학술지 이력

    학술지 이력
    연월일 이력구분 이력상세 등재구분
    2027 평가 재인증평가 신청대상 (재인증)
    2021-01-01 등재 등재학술지 유지 (재인증) KCI등재
    2018-06-08 학회명변경 한글명 : 국민체육진흥공단 부설 한국스포츠개발원 -> 국민체육진흥공단 한국스포츠정책과학원 KCI등재
    2018-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2017-04-11 학회명변경 영문명 : 미등록 -> Korea Institute of Sport Science KCI등재
    2015-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2014-03-24 학회명변경 한글명 : 국민체육진흥공단 체육과학연구원 -> 국민체육진흥공단 부설 한국스포츠개발원 KCI등재
    2013-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2010-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2008-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2006-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2005-07-01 학술지등록 한글명 : 체육과학연구
    외국어명 : Korean Journal of Sport Science
    KCI등재
    2003-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2002-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2001-07-01 등재 등재후보학술지 선정 (신규평가) KCI등재후보
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    학술지 인용정보

    학술지 인용정보
    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 0.78 0.78 0.84
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    0.8 0.84 0.781 0.21
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