心不全患者の運動耐容能と細胞レベルでの乳酸移送蛋白発現量との関連に関する研究

心力衰竭患者细胞水平运动耐量与乳酸转运蛋白表达水平关系的研究

基本信息

  • 批准号:
    12670054
  • 负责人:
  • 金额:
    $ 2.11万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2000
  • 资助国家:
    日本
  • 起止时间:
    2000 至 2001
  • 项目状态:
    已结题

项目摘要

It has been shown that there are lactate transporter proteins (monocarboxylate transporters : MCT) in the cell membranes of many tissues such as heart, skeletal muscle and red blood cells (RBCs). Seven MCT subtypes have been cloned in recent years. They are specifically distributed among tissues, RBCs, and musde fiber types. Although MCT1 in RBCs can be measured by blood samples, its significance has not been clarified. Firstly we made the polydonal anti-MCT1 antibody by immunizing against rabbits with synthetic peptide (11 amino adds) corresponding to the C-terminal of the human MCT1 molecule. With this antibody we examined the relationship between MCT1 in RBCs and exercise performance. 1) Twelve men (middle or long-distance runners) performed treadmill exercise (with 10% sloop) with stepwise protocol (0.5km/hr/ 3min). The subjects exercised to the point at which blood lactate concentrations were over 4.5 mmol/L; To evaluate exercise performance, we measured running speed at the onset of blood lactate accumulation of 4.0 mmol/L (OBLA). MCT1 in RBCs was measured by blood sample at rest. Results: The speed at the OBIA was 155± 1.3 (km/hr:mean±SD). MCT1 in RBCs was 80.1±41.6 (area density). There was a significant inverse correlation between them (r=-O.73, p<0.01). 2) Eight male student athletes and four Patients with CHF were studied about relationship between MCT andexercise tolerance (peak VO2). Results: There was a significant inverse correlation between MCT and peak V02 as a whole(r=-0.87,p=0.086)Conclusions: The results suggest that MCT1 in RBC play an important role in lactate-transport and might have a great role in determining exercise capacity of both normal persons and patients with CHF.
研究表明,许多组织如心脏、骨骼肌和红细胞(RBC)的细胞膜中存在乳酸转运蛋白(单羧酸转运蛋白:MCT)。近年来已克隆了7种MCT亚型。它们特异性地分布在组织、RBC和肌纤维类型中。虽然RBC中的MCT 1可以通过血液样本测量,但其意义尚未阐明。首先,我们用人工合成的人MCT 1分子C端11个氨基酸残基的多肽免疫家兔,制备了抗人MCT 1的多克隆抗体。使用该抗体,我们检查了RBC中的MCT 1与运动表现之间的关系。1)12名男子(中长跑运动员)进行跑步机运动(10%单桅纵帆船),逐步方案(0.5km/hr/3 min)。受试者运动到血乳酸浓度超过4.5 mmol/L的点;为了评估运动性能,我们测量了血乳酸累积4.0 mmol/L(OBLA)开始时的跑步速度。通过静息时的血液样本测量RBC中的MCT 1。结果:OBIA处的速度为155± 1.3(km/hr:平均值±SD)。红细胞中MCT 1的面积密度为80.1±41.6。两者呈显著负相关(r=-0.73,p = 0.01)。2)本文对8名男大学生运动员和4名CHF患者进行了MCT与运动耐量(峰值VO 2)关系的研究。结果如下:MCT与V02峰值呈负相关(r=-0.87,p = 0.086)。结论:红细胞MCT 1在乳酸转运中起重要作用,可能对正常人和CHF患者的运动能力有重要影响。

项目成果

期刊论文数量(4)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Okita K, Yonezawa K, Nishijima H et al.: "Muscle High-Energy Metabolite and Metabolic Capacity in Patients With Heart Failure"Med.Sci.Sport.Exerc.. 33-3. 442-448 (2001)
Okita K、Yonezawa K、Nishijima H 等:“心力衰竭患者的肌肉高能代谢物和代谢能力”Med.Sci.Sport.Exerc. 33-3。
  • DOI:
  • 发表时间:
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    0
  • 作者:
  • 通讯作者:
Okita.K: "Muscle High-Energy Metabolites and Metabolic Capacity in Patients with Heart Failure"Med.Sci.Sport.Exerc.. 33.3(in press). (2001)
Okita.K:“心力衰竭患者的肌肉高能代谢物和代谢能力”Med.Sci.Sport.Exerc.. 33.3(印刷中)。
  • DOI:
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    0
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  • 通讯作者:
Okita K, Yonezawa K, Nishijima H et al.: "Muscle High-Energy Metabolite and Metabolic Capacity in Patients With Heart Failure"Med. Sci. Sport. Exerc. 33-3. 442-448 (2001)
Okita K、Yonezawa K、Nishijima H 等:“心力衰竭患者的肌肉高能代谢物和代谢能力”Med。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Okita K, Yonezawa K, Nishijima H, et al.: "Muscle High-Energy Metabolite and Metabolic Capacity in Patients With Heart Failure"Med Sci. Sport. Exerc.. 33-3. 442-448 (2001)
Okita K、Yonezawa K、Nishijima H 等:“心力衰竭患者的肌肉高能代谢物和代谢能力”Med Sci。
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    0
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YONEZAWA Kazuya其他文献

YONEZAWA Kazuya的其他文献

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{{ truncateString('YONEZAWA Kazuya', 18)}}的其他基金

The relationship between biological responses to nitroglycerin and genotypes of the activating enzyme in human, and the application to personalized medicine
人体硝酸甘油生物反应与激活酶基因型的关系及其在个体化医疗中的应用
  • 批准号:
    20590553
  • 财政年份:
    2008
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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    1995
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    7782462
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    1995
  • 资助金额:
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