A role for polyamines in stimulus-secretion coupling in the pancreatic beta-cell.
Measurement of the content of polyamines in pancreatic islets indicated that no significant change in their concentration took place during glucose-stimulated insulin release. The finding, together with the absence of any effect of alpha-difluoromethylornithine on glucose-stimulated insulin release suggested that rapid synthesis of polyamines is not involved in stimulus-secretion coupling in the beta-cell. The concentration of polyamines found in islets were high enough for them to act as substrates for the Ca2+-dependent islet transglutaminase during insulin release. This was further demonstrated by the ability of islet transglutaminase to incorporate [14C]putrescine into proteins from islet homogenates and by the demonstration of an increase in the covalent incorporation of [14C]putrescine into the proteins of intact islets following their challenge with glucose. Unlike monoamine substrates of transglutaminase, putrescine failed to effectively inhibit insulin release when its intracellular concentration was increased. A role for polyamines in the secretory process through their incorporation into islet proteins is suggested.
D000217:Acyltransferases / Q000037:antagonists & inhibitors; D000818:Animals; D005260:Female; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000166:cytology / Q000378:metabolism*; D008297:Male; D065108:Ornithine Decarboxylase Inhibitors; D011073:Polyamines / Q000502:physiology*; D011700:Putrescine / Q000378:metabolism / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012636:Secretory Rate / Q000187:drug effects; D011503:Transglutaminases
D007328:Insulin; D065108:Ornithine Decarboxylase Inhibitors; D011073:Polyamines; D000217:Acyltransferases; D011503:Transglutaminases; D005947:Glucose; D011700:Putrescine