A low intake of long-chain polyunsaturated w3 fatty acids often prevails in Western population. The consequences of this situation in terms of the control of fuel homeostasis led us to explore metabolic, cationic and secretory variables in pancreatic islets from w3-depleted rats. The present study concerns the perturbation of Ca²⁺ fluxes and Ca²⁺-dependent insulin secretory events. Pancreatic islets were isolated from normal rats and w3-depleted rats. When required, the latter rats were injected intravenously 120 min before sacrifice with a medium chain triglyceride:fish oil emulsion (FO) or a control medium-chain triglyceride:olive oil emulsion (OO). The islets were incubated for 10-60 min for measurement of ⁴⁵Ca net uptake or 90 min for measurement of insulin release. The influx and fractional outflow rate of Ca²⁺ were both significantly lower and the steady-state ⁴⁵Ca labelling higher in OO-injected w3-depleted rats than in control animals. Prior injection of FO virtually normalized the latter but not the two former variables. The release of insulin evoked by 8.3 mM D-glucose at 1.0 mM Ca²⁺, when expressed relative to that found at either 2.8 mM D-glucose and 1.0 mM Ca²⁺ or 8.3 mM D-glucose in the absence of Ca²⁺, was much higher in the OO-injected as compared to FO-injected w3-depleted rats. Such was also the case under a number of other experimental conditions selected to affect Ca²⁺ fluxes in the islets. These findings suggest an impairment of Ca²⁺ inflow and an alteration of endogenous Ca²⁺ stores in w3-depleted rats, the latter anomaly being reversed within 120 min after the intravenous injection of the FO emulsion.