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

¹Laboratory of Experimental Hormonology, Brussels Free University, Brussels, Belgium; ²Département d'Alimentation Humaine, Institut National de la Recherche Agronomique, Clermont-Ferrand, France; and ³Laboratory of Experimental Surgery and ⁴Laboratory of Pharmacology, Brussels Free University, Brussels, Belgium

Submitted 9 September 2005 ; accepted in final form 24 March 2006

Considering the insufficient supply of long-chain polyunsaturated -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 -3-depleted rats. In terms of ⁴⁵Ca²⁺ handling, the islets from -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 ⁴⁵Ca²⁺-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 -3-poor MCT-olive oil (MCT:OO) emulsion. At 8.3 mM D-glucose, insulin release was higher in islets from -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 -3-depleted rats injected with the MCT:OO compared with the MCT:FO emulsion. A comparable situation prevailed when comparing islets from noninjected -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 -3-depleted rats.

long-chain polyunsaturated -3 fatty acid-depleted rats; calcium fluxes; pancreatic islets