Second-generation rats depleted in long-chain polyunsaturated omega3
fatty acids were recently proposed as a novel animal model for the
metabolic syndrome. In the present study, a dietary deprivation of omega3
acids for 3-7 months was found sufficient to provoke in 6-week-old normal rats the same alteration of the
fatty acid content and profile of liver
phospholipids and
triglycerides as that otherwise prevailing in the second-generation omega3-depleted rats, with emphasis on a severe decrease in their omega3
fatty acid content, alterations in the relative contribution of and ratio between selected long-chain polyunsaturated omega6
fatty acids, saturated and monodesaturated
fatty acids and precursors of
nervonic acid, and
liver steatosis. When the omega3-depleted rats were exposed, after the first 7 months of the present experiments and for 2-4 weeks to a diet supplemented with 5% (w/w)
flaxseed oil, most of these hepatic variables returned towards or beyond control values. In both the omega3-depleted rats and control animals, however, the eventual exposure to the
flaxseed oil-enriched diet failed to suppress
liver steatosis and, on the contrary, provoked a further increase in liver
triglyceride content. It is proposed, therefore, that the present approach represents a simple and realistic animal model to study the consequences of omega3-depletion. Moreover, the results suggest that to oppose such consequences, e.g.
liver steatosis, it may be necessary to combine the dietary supply of omega3
acids with a suitable control of food intake, in both qualitative and quantitative terms.