Synergism between vasopressin and phorbol esters in stimulation of insulin secretion and phosphatidylcholine metabolism in RIN insulinoma cells.
The tumor promoter, tetradecanoylphorbolacetate (TPA), causes a significant increase in both insulin secretion and the incorporation of 32Pi into phosphatidylcholine (PC) in RIN insulinoma cells. The peptide hormone, arginine vasopressin (AVP), also stimulates these functions, although to a lesser degree. When added together, the effects on secretion and PC metabolism are synergistic. At the same time, TPA inhibits the AVP-stimulated rise in phosphoinositide (PI) metabolism. Neither phloretin nor tamoxifen, reported to be inhibitors of protein kinase C activity, are able to block the effects of TPA on secretion, although both influence PC metabolism.
Monaco
M E
ME
Department of Physiology and Biophysics, New York University Medical Center, NY 10016.
Levy
B L
BL
Richardson
S B
SB
D007516:Adenoma, Islet Cell / Q000378:metabolism*; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D002460:Cell Line; D004357:Drug Synergism; D007340:Insulinoma / Q000378:metabolism*; D007700:Kinetics; D010190:Pancreatic Neoplasms / Q000378:metabolism*; D010693:Phloretin / Q000494:pharmacology; D010713:Phosphatidylcholines / Q000378:metabolism*; D051381:Rats; D013629:Tamoxifen / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D010713:Phosphatidylcholines; D013629:Tamoxifen; D001127:Arginine Vasopressin; D013755:Tetradecanoylphorbol Acetate; D010693:Phloretin