Abstract
Platelet activity is increased in persons with insulin dependent diabetes mellitus (IDDM). Receptor-medicated phospholipase C (PLC) activitation and hydrolysis of phosphatidylinositol bisphosphate (PIP 2) accompanies platelet activation. Previous work from our laboratory has shown that PIP 2 hydrolysis is decreased in platelets of persons with IDDM. PIP 2 hydrolysis is mediated via a phosphoinositide(PI)-specific PLC. PI-PLC activity is regulated by guanine nucleotide(GTP)-binding proteins. We therefore examined the hypothesis that platelet aggregations and PI turnover in platelet from subjects with IDDM is linked to alterations in PI-specific PLC activity. We found thrombin induced platelet aggregation was increased in the IDDM group. Basal PI and PIP 2-specific PLC activity was not statistically different for the two groups. Guanine-nucleotide stimulated PIP 2-specific PLC activity was decreased in the IDDM platelets. The mechanism for the reduced PLC activity and its role in the platelet hyperaggregation requires further study.
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