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1 Center for Cardiovascular Research, Department of Physiology, University of Illinois at Chicago, Chicago, IL, USA; Department of Biophysics, University of Illinois at Chicago, Chicago, IL, USA
2 Center for Cardiovascular Research, Department of Physiology, University of Illinois at Chicago, Chicago, IL, USA; Center for Cardiovascular Research, Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: pdetombe{at}uic.edu.
Cardiac disease in diabetes presents as impaired left ventricular contraction and relaxation, however the mechanisms underlying contractile protein dysfunction during the progression of disease are unknown. Accordingly, we assessed calcium dependent tension development and tension dependent ATP consumption (tension cost) in a rat model early (6 wk) and late (12 wk) following the onset of diabetes (50 mg/kg IV streptozotocin) using mechanical
force and enzyme coupled UV absorbance measurements. Myofilament calcium sensitivity and maximal tension was unchanged between groups at either time point. Cross-bridge cycling rate was significantly decreased in diabetes, as indexed by tension cost [Early: Control 5.4 ± 0.4
Diabetes 4.2 ± 0.3 Late: Control 6.0 ± 0.2 Diabetes 4.2 ± 0.2; p < 0.05]. Since rodent models of cardiac disease are confounded by altered myosin isoform distribution, myosin content was determined by SDS-PAGE and densitometry. The cardiac content of 
-myosin in diabetes was decreased to 41% ± 4.1at 6 weeks and 32.5% ± 2.9 at 12 weeks of diabetes (Control 6 weeks: 77.8 % ± 3.3 12 weeks: 73.6% ± 2.5 ). Separate control experiments demonstrated a linear decrease in tension cost with decreased -myosin content. Given this, the depression of tension cost in this rodent model of diabetes could be fully explained by the altered myosin isoform distribution.
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