Decreased capacity to inhibit platelet hyperactivity and to stabilize prostacyclin of high-density lipoproteins in experimental diabetes
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Twenty-eight male Sprague Dawley rats were divided into two groups: a control group (C) of 15 animals and a streptozotocin-induced diabetes group mildly balanced by insulin (D) of 13 animals. After 15 weeks, plasma and high-density lipoprotein (HDL) lipids were determined in each group. Apoprotein A-I concentration was evaluated in HDL fractions. The capacity of the HDL fraction to inhibit thrombin and ADP-induced aggregation of normal platelets was determined for each rat, and in an additional experiment the relation dose-effect of HDL was established. The effect of HDL of the two groups on the stabilization of prostacyclin was compared by aggregation bioassay. After 15 weeks, HDL cholesterol (free+esterified) tended to increase in group D compared with group C (P<0.08). By contrast, apoprotein A-I was very significantly decreased in HDL-D compared with HDL-C (P<0.001). These alterations were accompanied by a significantly decreased capacity of HDL (60 μg/ml platelet suspension) to inhibit ADP-induced aggregation (P<0.0001) in group D compared with group C. Furthermore, HDL-D incubated 45 or 90 min with prostacyclin showed a significantly decreased capacity to stabilize prostacyclin compared with HDL-C (P<0.04;P<0.03, respectively). These alterations in HDL could be involved in thrombosis and atheromatous complications associated with this disease.
Key wordsStreptozotocin-induced diabetic rats Highdensity lipoprotein Platelet aggregation Prostacyclin stabilization
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