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增加了腺单酸盐激活蛋白激酶活性在老鼠心脏与压力过载缩

R Tian¹, N Musi, J D'Agostino

¹NMR Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. rtian@rics.bwh.harvard.edu

|October 3, 2001

概括

过度缩的心脏中的慢性能量变化增加了腺单酸盐 (AMP) 激活蛋白激酶 (AMPK) 的活性,改变了葡萄糖的吸收. 这表明AMPK信号调节了这些条件下的基质使用.

科学领域:

心脏病学心脏病学
生物化学生物化学
分子生物学分子生物学

背景情况:

细胞能量状态的急性变化激活AMP激活蛋白激酶 (AMPK),影响肌肉中的基质利用.
左心室缩 (LVH) 涉及到心肌能量的慢性改变.
假设AMPK激活可以调节LVH心脏中的基质利用率.

研究的目的:

为了研究肌心能量的慢性变化与心脏过度缩中的AMPK活性之间的关系.
要确定AMPK是否在LVH的背景下调节基质利用.

主要方法:

利用 (31) P NMR 光谱和生化分析来分析心肌能量.
测量了腺三酸盐 (ATP),脂蛋白和总肌酸度.
评估的AMPK活性和表达,包括α1) 和α2) 异型.
量化2-脱氧葡萄糖的摄取量和葡萄糖输送物水平.

主要成果:

心脏的LVH显示ATP和脂蛋白减少,AMP/ATP比率增加.
在LVH中,AMPKα ((1) 和α ((2) 的活性显著升高.
在LVH中,AMPK的α(1) 表达增加,而α(2) 表达减少.
在LVH中,基础2-脱氧葡萄糖摄取量和血膜葡萄糖载体水平显著增加.

结论:

在LVH中心肌能量的慢性变化与AMPK活性升高有关.
在过度缩的心脏中,AMPK表达的异形特异性变化发生.
在LVH中,AMPK信号可能在调节基质利用方面起着至关重要的作用.

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