A Study on the Cardiac Myofibrillar ATPase Activity in Diabetic Rats.
10.4070/kcj.1987.17.3.479
- Author:
Wang Seong RYU
;
Un Ho RYOO
;
Jung Don SEO
;
Young Woo LEE
- Publication Type:Original Article
- Keywords:
Diabetic Cardiomyopathy;
Streptozotocin-induced diabetes;
Rat myocardium;
Myofibrillar ATPase activity
- MeSH:
Actins;
Actomyosin;
Adenosine Triphosphatases*;
Animals;
Cardiomyopathies;
Contractile Proteins;
Diabetes Mellitus;
Diabetic Cardiomyopathies;
Electrophoresis;
Heart;
Injections, Intravenous;
Ions;
Myocardium;
Myofibrils;
Myosin Heavy Chains;
Phosphates;
Rats*;
Sodium;
Streptozocin;
Troponin
- From:Korean Circulation Journal
1987;17(3):479-490
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Diabetes mellitus is known to be associated with a specific cardiomyopathy. This is evident from the clinical-pathological work and the epidemiologic data. An investigation was made in this study to determine whether diabetic cardiomyopathy in rats is associated with an alteration of biochemical characteristics of cardiac contractile proteins. Rats were made diabetic with intravenous injection of streptozotocin and hearts removed 8 weeks later for the isolation of myofibrils. The basal ATPase activity of myofibrils from diabetic hearts was significantly lower than that of the controls, suggesting the presence of some subtle structural and conformational changes in diabetic myofibrils. The activating effect of Mg ions on the myofibrillar actomyosin system of rat heart muscle was also demonstrated. Sodium dodecylsulfate gel electrophoresis showed the presence of myosin heavy chain, light chain 1 and 2, actin and troponin but failed to reveal differences in the patterns of these contractile proteins of light subunits between diabetics and controls. The deficiency in utilization of energy rich phosphates by the myofibrillar protein may be one of of the main mechanisms of cardiodepression observed in diabetic hearts. The cardiac myofibrillar ATPase activity may be one of useful measurements in evaluating pathophysiological states of cardiac contractile proteins.
