The mechanism of arachidonic acid-induced insulin secretion from rat islets of Langerhans.
The stimulation of rat pancreatic islets by glucose leads both to the secretion of insulin, and the production of arachidonic acid (AA). We have previously shown that exogenous AA can stimulate insulin secretion and that this secretion was not dependent upon extracellular Ca2+ nor upon the activation of protein kinase C. We have now demonstrated that AA-induced insulin secretion was a saturable and reversible process. AA-stimulated insulin secretion was slow in onset from intact islets but immediate from electrically permeabilized islets. In permeabilized islets AA-induced insulin secretion was not dependent on changes in intracellular Ca2+ or ATP and was not inhibited by noradrenaline. These results suggest that AA affects insulin secretion at a late stage in the exocytotic process.
Band
A M
AM
Biomedical Sciences Division, King's College London, UK.
Jones
P M
PM
Howell
S L
SL
D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D019301:Oleic Acid; D009829:Oleic Acids / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D007328:Insulin; D008041:Linoleic Acids; D009829:Oleic Acids; D016718:Arachidonic Acid; D019301:Oleic Acid; D019787:Linoleic Acid; D009638:Norepinephrine