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1 Division of Pharmacology and Toxicology, The University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: rodrigue{at}interchange.ubc.ca.
Diabetic patients are particularly susceptible to cardiomyopathy independent of vascular disease, and recent evidence implicates cell death as a contributing factor. Given its protective role against apoptosis, we hypothesized that dietary n-6 polyunsaturated fatty acid (PUFA) provision may well decrease the incidence of this mode of cardiac cell death following diabetes. Male Wistar rats were first fed a diet rich in n-6 PUFA [20% w/w sunflower oil] for 4 weeks followed by 55 mg/kg streptozotocin (STZ) to induce diabetes. Following a brief period of hyperglycemia (4 days), hearts were excised for functional, morphological, and biochemical analysis. In diabetic rats, n-6 PUFA decreased caspase-3 activity, crucial for myocardial apoptosis. However, cardiac necrosis, an alternative mode of cell death increased. In these hearts, a rise in linoleic acid and depleted cardiac glutathione could explain this 'switch' to necrotic cell death. Additionally, mitochondrial abnormalities, impaired substrate utilization and enhanced triglyceride accumulation could have also contributed towards a decline in cardiac function in these animals. Our study provides evidence that unlike other models of diabetic cardiomyopathy that exhibit cardiac dysfunction only after chronic hyperglycemia, n-6 PUFA feeding coupled with only four days of diabetes precipitated metabolic and contractile abnormalities in the heart. Thus, although promoted as being beneficial, excess n-6 PUFA with its predisposition to induce obesity, insulin resistance and ultimately diabetes, could accelerate myocardial abnormalities in diabetic patients.
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