ストレプトゾトシン誘発糖尿病心におけるミオシン重鎖の質的・量的変化

Qualitative and Quantitative Change of Myosin Heavy Chain in Streptozotocin-induced Diabetic Rat Hearts

　糖尿病は心機能低下の重要な要因の一つであるが，糖尿病性心の心筋構造タンパク質の変化についてはほとんど知られていない．糖尿病心における心筋構造タンパク質の質的・量的変化を調べるために，streptozotocin（STZ）誘発糖尿病ラットを作成した．ミオシン重鎖アイソザイムの変化をSDS-PAGEを用い，二次元電気泳動法を用いて心筋構造タンパク質含量を測定した．STZ注射後6週では，ミオシン重鎖はα鎖からβ鎖に変化した．15週後では低いATPase活性を持つβ鎖が著明となり，ミオシン重鎖含量はコントロール群に比較し減少した．ミオシン重鎖がATPase活性をもつことを考慮すると，ミオシン重鎖アイソザイムの変化とミオシン重鎖含量の減少は糖尿病状態における心機能低下を起こすと思われた．

Diabetes mellitus is one cause of myocardial dysfunc-tion, but little was hnown about change of cardiac structural proteins in diabetic cardiomyopathy. In order to investigate the qualitative and quantitative changes of structural proteins in the rat hearts, we made streptozotocin (STZ)-induced diabetic rats We analyzed the shift of myosin heavy chain (MHC) is-ozyme by SDS-PAGE and determined the contents of the cardiac structural proteins by two-dimensional electrophoresis.

Six weeks after STZ injection, the patterns of MHC on polyacrylamide gels were shifted from a a pattern to a β pattern and the β MHC isozyme, which has a low ATPase activity, had become the predominant isozyme pattern at 15 weeks. Fifteen weeks after, the content of MHC in STZ rats decreased as compared with that in controls. Indicating that MHC has an ATPase activity, the shift of MHC isozyme and the decrease of the content of MHC can explain abnormality of cardiac dysfunction in diabetic rat hearts.