The impaired synthesis of insulin and its inability to inhibit platelet aggregation in cerebrovascular accident.

Abstract

Both ischemic stroke (IS) and hemorrhagic stroke (HS) are reported to occur due to thrombosis on the arteries of the brain. As diabetes mellitus is a risk factor for strokes and insulin is reported to prevent thrombosis, the role of insulin in IS and HS was investigated. Forty eight stroke victims (IS=22, HS=26) and equal number of aged and sex matched normal volunteers participated in the study. Nitric oxide was determined by methemoglobin method. Insulin and Dermcidin isoform-2 (DCN2) level was determined by ELISA by using insulin and dermcidin antibody. Insulin binding to the platelet membrane was analyzed by scat chard plot. Treatment of normal platelet rich plasma (10(8)platelets/ml) with 15μUnits insulin/ml produced 1.41nmol NO. The PRP from the IS and HS victims produced 0.38nmol NO and 0.08nmol NO respectively. Pretreatment of PRP from IS or HS subjects with 15μM aspirin followed by 15μUnits of insulin/ml resensitized the platelets to the inhibitory effect of insulin. Mice hepatocytes treated with 0.14μM DCN2 abolished the glucose induced insulin synthesis by NO that can be reversed by using 15μM aspirin. It can be concluded that presence of DCN2 in stroke causes a condition similar to type I diabetes and nullified the effect of insulin in the inhibition of platelet aggregation in both IS and HS. The effect was reversed by 15μM aspirin.