Acute diabetes does not reduce heparin-releasable lipoprotein lipase activity in perfused hearts from Wistar–Kyoto rats

Abstract

The induction of diabetes (3–5 days duration) in Wistar–Kyoto rats by the administration of streptozotocin (100 mg/kg) did not increase plasma concentrations of triacylglycerols or free fatty acids, and did not reduce heparin-releasable (functional) lipoprotein lipase activity in perfused hearts. By comparison, diabetic Sprague–Dawley rats were characterized as having hypertriglyceridemia and decreased heparin-releasable lipoprotein lipase activity in perfused hearts. Therefore, the diabetes-induced reduction in myocardial lipoprotein lipase activity in Sprague–Dawley rat hearts may, at least in part, be a compensatory response to the hypertriglyceridemia and increased fatty acid delivery to the myocardial cell, which is a characteristic feature of most severe, insulin-deficient models of diabetes mellitus. Although functional, endothelium-bound lipoprotein lipase activity was not reduced in diabetic perfused hearts from Wistar–Kyoto rats, cellular and heparin-releasable lipoprotein lipase activity was reduced in cardiac myocyte preparations, suggesting that other mechanisms in addition to plasma triacylglycerol must regulate lipoprotein lipase activity in the whole diabetic Wistar–Kyoto rat heart and that cardiac myocytes may not be the exclusive source of functional lipoprotein lipase in the diabetic myocardium.Key words: diabetes, hypertriglyceridemia, lipoprotein lipase, perfused hearts, cardiac myocytes.