L-glutamine and palmitate catabolism in pancreatic islets from rats depleted in long-chain polyunsaturated ω3 fatty acids

The catabolism of D-glucose was recently found to be impaired in pancreatic islets from rats depleted in long-chain polyunsaturated omega 3 fatty acids. The specificity of this alteration was now investigated by characterizing the oxidative fate of endogenous nutrients in islets preincubated with either L-[U-C-14] glutamine or [U-C-14] palmitate and then incubated variously in the absence Of D-glucose, presence of the hexose or presence of metabolic poisons. Relative to their radioactive content after preincubation, the production of (CO2)-C-14 by islets prelabelled with [U-C-14] glutamine was higher in omega 3-depleted rats than control animals. The enhancing action of D-glucose upon such production was impaired, however, in the omega 3-depleted rats. The net uptake of C-14-palmitate and absolute value for (CO2)-C-14 output were both increased in omega 3-depleted rats, whilst the ratio between (CO2)-C-14 output and islet radioactive content was decreased in the same animals. The inhibition of (CO2)-C-14 production by metabolic poisons was comparable in all cases. These results are consistent with recent findings on such items as the availability of endogenous amino acids and uptake of unesterified fatty acids in extrapancreatic sites of the omega 3-depleted rats. They also support the view that the alteration of D-glucose metabolism in the islets of the latter animals may be attributable, in part at least, to alteration of glucokinase kinetics by high intracellular acyl-CoA levels. Copyright (C) 2007 John Wiley & Sons, Ltd.