We examined the formation of sphingolipid mediators in platelets, which abundantly store, and release extracellularly, sphingosine 1-phosphate (Sph-1-P). Challenging [(3)H]Sph-labeled platelet suspensions with thrombin or 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in a decrease in Sph-1-P formation and an increase in sphingosine (Sph), ceramide (Cer), and sphingomyelin formation. Sph conversion into Cer, and Cer conversion into sphingomyelin were not affected upon activation, suggesting that Sph-1-P dephosphorylation may initiate the formation of sphingolipid signaling molecules.
View Article and Find Full Text PDFNihon Rinsho Meneki Gakkai Kaishi
February 2003
The patient is a 71-year-old woman who underwent splenectomy after the diagnosis of idiopathic portal hypertension (IPH) at the age of 51 years. Thirst and polyuria occurred in December 1995. In April 1996, she was hospitalized for assessment because of elevation of her blood glucose and HbA1c levels to 535 mg/dl and 14.
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