Effect of insulin treatment on prostacyclin in experimental diabetes

Abstract

Diabetic patients have a high susceptibility to microvascular complications, atherosclerosis and thrombosis. Platelet hyperreactivity possibly related to an imbalance in arachidonic acid metabolism may be involved. Aortic rings or renal cortex produced a potent inhibitor of platelet aggregation, identified as prostacyclin (PGI₂). Release of PGI₂ by tissues from streptozotocin — diabetic rats (aorta: 0.07±0.1 ng/ mg wet weight; renal cortex 0.004±0.001 ng/mg wet weight) was significantly depressed when compared with controls (aorta: 0.26±0.07 ng/mg wet weight; renal cortex: 0.009±0.001 ng/mg wet weight). Treatment of diabetic animals with insulin for 8 days restored PGI₂ production to normal. The finding that PGI₂ is depressed in the aorta and in the kidney, tissues which develop angiopathy, and that this is normalised by insulin, suggests that impaired PGI₂ production, perhaps associated with platelet hyperreactivity may play a role in the vascular complications of diabetes.