Creatine kinase kinetics in diabetic cardiomyopathy.
Matsumoto, Yuji, Md, Masanori Kaneko, Md, Phd, Akira Kobayashi, Md,
Phd, Yutaka Fujise, Phd, and Noboru Yamazaki, Md, Phd.
The Third Department of Internal Medicine and Chemistry, Hamamatsu
University School of Medicine, 3600 Handa-cho, Hamamatsu, 431-31,
Japan
APStracts 2:0014E, 1995.
One feature of the diabetic cardiomyopathy is the appearance of
contractile dysfunction as the workload increases. We hypothesized
that this resulted from an impaired creatine kinase / phosphocreatine
system and, therefore, examined the creatine kinase kinetics at both
low and high workloads. Creatine kinase flux ( by 31P-NMR saturation
transfer method ), cardiac performance and oxygen consumption were
measured in control and streptozotocin-induced diabetic rat hearts.
Creatine kinase flux was inhibited by iodoacetamide in control hearts
to confirm the role of the creatine kinase / phosphocreatine system
in cardiac performance. In diabetic hearts, (1) the contractile
dysfunction became apparent only at high workloads, (2) the ATP
synthesis rate was not significantly different from control hearts,
(3) the creatine kinase flux was reduced by 30.8% ( 257.5 7.7 mol/g
wet wt/min in control vs. 178.3 9.4 in diabetes, P< 0.001 ) and (4)
the creatine kinase flux did not increase as the workload increased.
In control hearts, (5) iodoacetamide inhibited the creatine kinase
flux to the same degree as that in diabetic hearts and (6) the
contractile dysfunction was not as severe as that observed in
diabetic hearts. These results suggest that the impaired creatine
kinase / phosphocreatine system is, at least in part, responsible for
the contractile dysfunction in the diabetic cardiomyopathy.
Received 18 October 1994; accepted in final form 18 January 1995.
APS Manuscript Number E430-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.