Abstract
1,2-Didecanoylglycerol (diC10) is taken up by human platelets and sequentially converted to 1,2-didecanoyl-phosphatidic acid (PA10) and 1,2-didecanoylphosphatidylinositol (PI10). Agents that increase cyclic AMP in platelets, such as prostacyclin and forskolin, sequentially convert diC10 to pa10 and PI10. They decrease formation of PA10 with a parallel accumulation of PI10. This might reflect an inhibition of phosphatidylinositol kinase.