Pancreatic islet function in omega-3 fatty acid-depleted rats : Alteration of calcium fluxes and calcium-dependent insulin release

Considering the insufficient supply of long-chain polyunsaturated omega-3 fatty acids often prevailing in Western populations, this report deals mainly with alterations of Ca2+ fluxes and Ca2+-dependent insulin secretory events in isolated pancreatic islets from omega-3-depleted rats. In terms of Ca-45(2+) handling, the islets from omega-3-depleted rats, compared with those from normal animals, displayed an unaltered responsiveness to an increase in extracellular K+ concentration, a lower inflow rate and lower fractional outflow rate of the divalent cation, and higher Ca-45(2+)-labeled cellular pool(s) at isotopic equilibrium. The latter anomaly was corrected 120 min after intravenous injection of a novel medium-chain triglyceride-fish oil (MCT:FO) emulsion, distinct from a control omega-3-poor MCT-olive oil (MCT:OO) emulsion. At 8.3 mM D-glucose, insulin release was higher in islets from omega-3-depleted rats vs. control animals, coinciding with a higher cytosolic Ca2+ concentration. The relative magnitude of the increase in insulin output attributable to a rise in D-glucose as well as extracellular Ca2+ or K+ concentration, to the absence vs. presence of verapamil and to the presence vs. absence of extracellular Ca2+, theophylline, phorbol 12-myristate 13-acetate, or Ba2+, was always more pronounced in islets from omega-3-depleted rats injected with the MCT: OO compared with the MCT: FO emulsion. A comparable situation prevailed when comparing islets from noninjected omega-3-depleted and normal rats. In light of these and previous findings, we propose that an impairment of Na+, K+-ATPase activity plays a major, although not an exclusive, role in the perturbation of Ca2+ fluxes and Ca2+-dependent secretory events in the islets from omega-3-depleted rats.