Insulin secretion without the participation of arachidonic acid.
In order to study the role of arachidonic acid (AA) in depolarization-induced insulin secretion rat insulinoma cells (RINm5F) were depleted of AA by cultivation in essential fatty acid-free medium. Within 2 weeks AA content of these cells was decreased to a non-detectable level as assessed by gas chromatography (GC). Different cell lines were obtained by supplementation of the defatted medium with oleic acid or the AA precursor linoleic acid (7 and 70 microM, each). The AA content varied in dependence from the precursor availability from 0 to about 14% of long chain fatty acids. Variation in AA content or the depletion of AA to a non-detectable level did not modulate insulin synthesis, basal and potassium-induced insulin release, cell growth (cell number and protein), membrane depolarization and increases in cytosolic Ca2+. In AA containing cells no eicosanoids was produced in the course of stimulated hormone release. The data suggest that in RINm5F cells release of AA and/or formation of oxidized metabolites from AA are not essential for functional integrity.
Safayhi
H
H
Department of Pharmacology, University of Tübingen, Germany.
Koopmann
I
I
Ammon
H P
HP
D000409:Alanine / Q000494:pharmacology; D000818:Animals; D016718:Arachidonic Acid / Q000502:physiology*; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002455:Cell Division; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007340:Insulinoma / Q000378:metabolism; D008084:Lipoxygenase / Q000378:metabolism; D008564:Membrane Potentials; D010190:Pancreatic Neoplasms / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D014407:Tumor Cells, Cultured
D007328:Insulin; D016718:Arachidonic Acid; D000001:Calcimycin; D011189:Potassium Chloride; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases; D000409:Alanine; D002118:Calcium