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    Changes of Muscle Insulin-like Growth Factor-I and Concentrations of Inflammatory Cytokines in Rat Skeletal Muscle Following Denervation and Diabetes-induced Atrophy

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    https://www.riss.kr/link?id=A103566797

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    [PURPOSE] Muscle atrophy is the result of several diseases and conditions. In systemic disease, many factors contribute to muscle atrophy. Insulin-like growth factor-I (IGF-I) is a local and systemic hormone that contributes to muscle growth. The aim of this study was to investigate the changes in muscle protein synthesis biomarkers and pro-inflammatory factors associated with muscle atrophy in systemic disease. [METHODS] Local muscle tissue damage was observed and compared in both streptozotocin (STZ) -induced diabetic and denervated rats. In these animal models, we measured the expression of muscle-specific IGF-1 (mIGF-1) in by real-time PCR and serum concentrations of inflammatory cytokines by ELISA. In addition, muscle mass and blood glucose levels were observed for six weeks. [RESULTS] The results showed that muscle mass was significantly lower in both experimental groups compared to the control group from week two. Over the six week period, muscle mass gradually increased in the control group, dramatically decreased in the denervated group, but interestingly, showed no significant changes in the diabetes group. Inflammatory factors including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly higher in diabetic rats than in the control group. The level of TNF-α was increased at week four; however, IL-6 levels did not change in denervated rats. The expression of mIGF-1 mRNA did not change significantly in the two experimental groups. [CONCLUSIONS] In conclusion, mIGF-1 for the proliferation of muscle cells did not have an effect on muscle atrophy among the groups. However the increase in systemic inflammatory factors may be involved in the process of muscle atrophy in diabetic rats.
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    [PURPOSE] Muscle atrophy is the result of several diseases and conditions. In systemic disease, many factors contribute to muscle atrophy. Insulin-like growth factor-I (IGF-I) is a local and systemic hormone that contributes to muscle growth. The aim ...

    [PURPOSE] Muscle atrophy is the result of several diseases and conditions. In systemic disease, many factors contribute to muscle atrophy. Insulin-like growth factor-I (IGF-I) is a local and systemic hormone that contributes to muscle growth. The aim of this study was to investigate the changes in muscle protein synthesis biomarkers and pro-inflammatory factors associated with muscle atrophy in systemic disease. [METHODS] Local muscle tissue damage was observed and compared in both streptozotocin (STZ) -induced diabetic and denervated rats. In these animal models, we measured the expression of muscle-specific IGF-1 (mIGF-1) in by real-time PCR and serum concentrations of inflammatory cytokines by ELISA. In addition, muscle mass and blood glucose levels were observed for six weeks. [RESULTS] The results showed that muscle mass was significantly lower in both experimental groups compared to the control group from week two. Over the six week period, muscle mass gradually increased in the control group, dramatically decreased in the denervated group, but interestingly, showed no significant changes in the diabetes group. Inflammatory factors including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly higher in diabetic rats than in the control group. The level of TNF-α was increased at week four; however, IL-6 levels did not change in denervated rats. The expression of mIGF-1 mRNA did not change significantly in the two experimental groups. [CONCLUSIONS] In conclusion, mIGF-1 for the proliferation of muscle cells did not have an effect on muscle atrophy among the groups. However the increase in systemic inflammatory factors may be involved in the process of muscle atrophy in diabetic rats.

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    참고문헌 (Reference)

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    2 Holly J. M. P., "The role of growth hormone in diabetes mellitus" 118 : 353-364, 1988

    3 Midrio M., "The denervated muscle: facts and hypotheses. A historical review" 98 : 1-21, 2006

    4 Philippou A., "The Role of the Insulin-like Growth Factor 1 (IGF-1) in Skeletal Muscle Physiology" 21 : 45-54, 2007

    5 Evans, W. J., "Skeletal muscle loss: cachexia, sarcopenia, and inactivity" 91 : 1123S-1127S, 2010

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    1 Adams G. R., "Time course of changes in markers of myogenesis in overloaded rat skeletal muscles" 87 : 1705-1712, 1999

    2 Holly J. M. P., "The role of growth hormone in diabetes mellitus" 118 : 353-364, 1988

    3 Midrio M., "The denervated muscle: facts and hypotheses. A historical review" 98 : 1-21, 2006

    4 Philippou A., "The Role of the Insulin-like Growth Factor 1 (IGF-1) in Skeletal Muscle Physiology" 21 : 45-54, 2007

    5 Evans, W. J., "Skeletal muscle loss: cachexia, sarcopenia, and inactivity" 91 : 1123S-1127S, 2010

    6 Glass D. J., "Skeletal muscle hypertrophy and atrophy signaling pathways" 37 : 1974-1984, 2005

    7 Bongers K. S., "Skeletal muscle denervation causes skeletal muscle atrophy through a pathway that involves both Gadd45a and HDAC4" 305 : E907-E915, 2013

    8 Egerman M. A., "Signaling pathways controlling skeletal muscle mass" 0 : 1-10, 2013

    9 Sandri M., "Signaling in Muscle Atrophy and Hypertrophy" 23 : 160-170, 2008

    10 Narici M. V., "Sarcopenia: characteristics, mechanisms and functional significance" 95 : 139-159, 2010

    11 Velloso C. P., "Regulation of muscle mass by growth hormone and IGF-I" 154 : 557-568, 2008

    12 Fan J., "Regulation of insulin-like growth factor (IGF)-I mRNA and peptide and IGF-binding proteins by interleukin-1" 270 : R621-R629, 1996

    13 Whitman S. A., "Nrf2 modulates contractile and metabolic properties of skeletal muscle in streptozotocin-induced diabetic atrophy" 319 : 2673-2683, 2013

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    20 Shavlakadze T., "Insulin-like growth factor I slows the rate of denervation induced skeletal muscle atrophy" 15 : 139-146, 2005

    21 Krause M. P., "Impaired Macrophage and Satellite Cell Infiltration Occurs in a Muscle-Specific Fashion Following Injury in Diabetic Skeletal Muscle" 8 : e70971-, 2013

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    25 Eliakim A., "Fitness, Training, and the Growth Hormone→Insulin-Like Growth Factor I Axis in Prepubertal Girls" 86 : 2797-2802, 2001

    26 Gosteli-Peter M. A., "Expression and regulation of insulin-like growth factor-I (IGF-I) and IGF-binding protein messenger ribonucleic acid levels in tissues of hypophysectomized rats infused with IGF-I and growth hormone" 135 : 2558-2567, 1994

    27 Masiello P., "Experimental NIDDM: Development of a New Model in Adult Rats Administered Streptozotocin and Nicotinamide" 47 : 224-229, 1998

    28 Yach D., "Epidemiologic and economic consequences of the global epidemics of obesity and diabetes" 12 : 62-66, 2006

    29 Punkt K., "Effects on skeletal muscle fibres of diabetes and Ginkgo biloba extract treatment" 101 : 53-69, 1999

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    33 Muller F. L., "Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production" 293 : R1159-R1168, 2007

    34 Jaweed M. M., "Denervation and reinnervation of fast and slow muscles. A histochemical study in rats" 23 : 808-827, 1975

    35 Midrio M., "Cordotomy-denervation interactions on contractile and myofibrillar properties of fast and slow muscles in the rat" 100 : 216-236, 1988

    36 Barbieri M., "Chronic inflammation and the effect of IGF-I on muscle strength and power in older persons" 284 : E481-E487, 2003

    37 Brownlee M., "Biochemistry and molecular cell biology of diabetic complications" 414 : 813-820, 2001

    38 Reid M. B., "Beyond atrophy: redox mechanisms of muscle dysfunction in chronic inflammatory disease" 589 : 2171-2179, 2011

    39 Hu G., "Association of Serum C-Reactive Protein Level with Sex-Specific Type 2 Diabetes Risk: A Prospective Finnish Study" 94 : 2099-2105, 2009

    40 Pellegrino C., "An electron microscope study of denervation atrophy in red and white skeletal muscle fibers" 17 : 327-349, 1963

    41 Wohaieb S. A., "Alterations in free radical tissue-defense mechanisma in streptozotocin-induced diabetic rats" 36 : 1014-1018, 1987

    42 DeVol D. L., "Activation of insulin-like growth factor gene expression during work-induced skeletal muscle growth" 259 : E89-E95, 1990

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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
    2018-01-31 학술지명변경 한글명 : 운동학 학술지 -> 아시아 운동학 학술지
    외국어명 : The Journal of Kinesiology -> The Asian Journal of Kinesiology
    KCI등재
    2018-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2017-02-09 학술지명변경 외국어명 : The Official Journal of the Korean Academy of Kinesiology -> The Journal of Kinesiology KCI등재
    2015-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2014-09-18 학술지명변경 외국어명 : 미등록 -> The Official Journal of the Korean Academy of Kinesiology KCI등재
    2011-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2010-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2008-01-01 등재 등재후보학술지 선정 (신규평가) KCI등재후보
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    학술지 인용정보

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    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 0.57 0.57 0.66
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    0.63 0.67 0.686 0.03
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