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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Creatine kinase kinetics in diabetic cardiomyopathy
Y Matsumoto1, M Kaneko, A Kobayashi
1Third Department of Internal Medicine and Chemistry, Hamamatsu University School of Medicine, Japan.
The American Journal of Physiology
|June 1, 1995
Summary
Diabetic cardiomyopathy impairs heart function, especially under high workload. This study reveals that an impaired creatine kinase/phosphocreatine system is a key factor contributing to this contractile dysfunction in diabetic hearts.
Area of Science:
- Cardiovascular Physiology
- Metabolic Diseases
- Biochemistry
Background:
- Diabetic cardiomyopathy is characterized by contractile dysfunction that worsens with increased workload.
- The creatine kinase/phosphocreatine system is crucial for cellular energy buffering in the heart.
Purpose of the Study:
- To investigate the role of the creatine kinase/phosphocreatine system in the development of contractile dysfunction in diabetic cardiomyopathy.
- To examine creatine kinase kinetics under varying workloads in diabetic rat hearts.
Main Methods:
- Utilized 31P nuclear magnetic resonance saturation transfer to measure creatine kinase flux.
- Assessed cardiac performance and oxygen consumption in control and streptozotocin-induced diabetic rat hearts.
- Used iodoacetamide to inhibit creatine kinase flux in control hearts for comparison.
Main Results:
- Diabetic hearts exhibited contractile dysfunction primarily at high workloads.
- Creatine kinase flux was significantly reduced (30.8%) in diabetic hearts compared to controls.
- Inhibition of creatine kinase flux in control hearts mimicked the reduction seen in diabetic hearts, but with less severe contractile dysfunction.
Conclusions:
- An impaired creatine kinase/phosphocreatine system contributes significantly to contractile dysfunction in diabetic cardiomyopathy.
- The energy buffering capacity of the heart is compromised in diabetes, leading to functional deficits under stress.
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