VASOPRESSIN AND OXYTOCIN BUT NOT GLUCOSE STIMULATE HYDROLYSIS OF PHOSPHATIDYLINOSITOL AND PHOSPHATIDYLCHOLINE IN A HAMSTER INSULINOMA

HIT-T15 cells prelabeled with [H-3]-arachidonate were incubated lor 15 minutes at 37-degrees-C in Krebs Ringer buffer (pH 7.1) in the presen ce and absence of various agonists. Radioactivity remaining in major p hospholipids was measured at the end of incubation period. Oxytocin (1 muM), vasopressin (1 muM), and A23187 (5 muM) stimulated loss of radi oactivity from phosphatidylinositol and phosphatidylcholine. No loss o f radioactivity from either of the phospholipids, however, was detecte d in the presence of 10 mM D-glucose, an insulin secretagogue in HIT-T 15 cells. The lack of phosphatidylinositol response to glucose was als o evident when the cells were prelabeled with myo-[H-3] inositol. The formation of inositol phos hates at 15 minutes was readily observed up on the treatment of myo-[H-3] inositol-labeled cells with oxytocin or vasopressin but not glucose or A23187. Inability of glucose to stimula te phosphatidylinositol and phosphatidylcholine hydrolysis in beta cel l-derived HIT-T15 cells contrasts sharply with results from studies wi th pancreatic islets. where hydrolysis of these two phospholipids is r eadily observed and thought to contribute to the signaling mechanism r esponsible for stimulation of insulin secretion.