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  • Title: Vasopressin and oxytocin but not glucose stimulate hydrolysis of phosphatidylinositol and phosphatidylcholine in a hamster insulinoma.
    Author: Gonzalez R, Rana RS.
    Journal: Life Sci; 1993; 53(15):1179-83. PubMed ID: 8412474.
    Abstract:
    HIT-T15 cells prelabeled with [3H]-arachidonate were incubated for 15 minutes at 37 degrees C in Krebs Ringer buffer (pH 7.1) in the presence and absence of various agonists. Radioactivity remaining in major phospholipids was measured at the end of incubation period. Oxytocin (1 microM), vasopressin (1 microM), and A23187 (5 microM) stimulated loss of radioactivity from phosphatidylinositol and phosphatidylcholine. No loss of radioactivity from either of the phospholipids, however, was detected in the presence of 10 mM D-glucose, an insulin secretagogue in HIT-T15 cells. The lack of phosphatidylinositol response to glucose was also evident when the cells were prelabeled with myo-[3H] inositol. The formation of inositol phosphates at 15 minutes was readily observed upon the treatment of myo-[3H] inositol-labeled cells with oxytocin or vasopressin but not glucose or A23187. Inability of glucose to stimulate phosphatidylinositol and phosphatidylcholine hydrolysis in beta cell-derived HIT-T15 cells contrasts sharply with results from studies with pancreatic islets, where hydrolysis of these two phospholipids is readily observed and thought to contribute to the signaling mechanism responsible for stimulation of insulin secretion.
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