Insulinotropic effect of the tumor promoter teleocidin in isolated pancreatic islets.
A tumor promoter teleocidin induced insulin secretion from isolated pancreatic islets in a concentration-dependent manner. The teleocidin-induced secretion was inhibited by p-bromophenacyl bromide, nordihydroguaiaretic acid, 3-amino-1-(3-trifluoromethylphenyl)-2-pyrazoline and 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone, but not by indomethacin. Insulinotropic concentrations of teleocidin stimulated 6-keto-prostaglandin F1 alpha release from pancreatic islets. These results suggest that phospholipase A2 activation and lipoxygenase product(s) are involved in the mechanism of teleocidin-induced insulin secretion.
D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008235:Lyngbya Toxins; D008297:Male; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D000470:Alkaloids; D002273:Carcinogens; D007328:Insulin; D008235:Lyngbya Toxins; D011448:Prostaglandin Antagonists; C022176:teleocidins; D007213:Indomethacin