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1 Department of Medical Physiology, Institute of Medical Biology, Faculty of Medicine, University of Tromsoe, Tromseo, Tromsoe, Norway
2 Department of Pharmacology and Therapeutics, Faculty of Medicine,, Canada, Alberta, Canada
* To whom correspondence should be addressed. E-mail: ellenaa{at}fagmed.uit.no.
Diabetic db/db mice provide an animal model of type 2 diabetes characterized by marked in vivo insulin resistance. The effect of insulin on myocardial metabolism has not been fully elucidated in this diabetic model. In the present study we tested the hypothesis that the metabolic response to insulin in db/db hearts will be diminished due to cardiac insulin resistance. Insulin-induced changes in glucose oxidation (GLUox) and fatty acid oxidation (FAox) were measured in isolated hearts from control and diabetic mice, perfused both with low as well as high consentration of glucose and FA: 10 mM glucose/0.5 mM palmitate and 28 mM glucose/1.1 mM palmitate. Both in the absence and presence of insulin, diabetic hearts showed decreased rates of GLUox and elevated rates of FAox. However, the insulin-induced increment in glucose oxidation as well as the insulin-induced decrement in FA oxidation was similar, or even more pronounced in diabetic that in control hearts. During elevated FA and glucose supply, however, the effect of insulin was blunted in db/db hearts with respect to both FAox and GLUox. Finally, insulin-stimulated deoxyglucose uptake was markedly reduced in isolated cardiomyocytes from db/db mice, while glucose uptake in isolated perfused db/db hearts was clearly responsive to insulin. These results show that, despite reduced insulin-stimulated glucose uptake in isolated cardiomyocytes, isolated perfused db/db hearts are responsive to metabolic actions of insulin. These results should advocate use of insulin therapy (glucose-insulin-potassium) in diabetic patients undergoing cardiac surgery or during reperfusion after an ischemic insult.
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