糖尿病大鼠心脏中的线粒体肌酸磷酸激酶缺乏症
Mitochondrial creatine phosphokinase deficiency in diabetic rat heart.
作者信息
Savabi F
机构信息
Department of Pharmacology and Nutrition, University of Southern California, School of Medicine, Los Angeles 90033.
出版信息
Biochem Biophys Res Commun. 1988 Jul 15;154(1):469-75. doi: 10.1016/0006-291x(88)90710-3.
The role of the mitochondrial end of the phosphocreatine energy shuttle was studied in the streptozotocin diabetic rat heart. Diabetic rats had 45 +/- 5% lower body weight and yielded 46 +/- 6% less mitochondria gm of protein than normals. Diabetic heart mitochondria had 32 +/- 7% lower creatine phosphokinase (CPK) activity and 59 +/- 10% lower oxygen consumption rate than normal heart mitochondria. Creatine (25 mM) did not stimulate oxygen uptake by diabetic heart although control (normal) heart mitochondria were stimulated. Inadequate mitochondrial energy production in the form of phosphocreatine could result in lower energy delivery to the myofibrillar contraction sites and might be an important factor in diabetic cardiomyopathy and weight loss.
在链脲佐菌素诱导的糖尿病大鼠心脏中，研究了磷酸肌酸能量穿梭的线粒体末端的作用。糖尿病大鼠的体重比正常大鼠低45±5%，每克蛋白质产生的线粒体比正常大鼠少46±6%。糖尿病心脏线粒体的肌酸磷酸激酶（CPK）活性比正常心脏线粒体低32±7%，耗氧率低59±10%。尽管对照（正常）心脏线粒体受到肌酸（25 mM）的刺激，但糖尿病心脏的氧摄取并未受到刺激。以磷酸肌酸形式产生的线粒体能量不足可能导致传递到肌原纤维收缩部位的能量减少，这可能是糖尿病心肌病和体重减轻的一个重要因素。
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