The influences of dietary linseed oil and saturated fatty acids on caecal enterocytes in Arctic char (Salvelinus alpinus L.): a quantitative ultrastructural study

Arctic char (Salvelinus alpinus L.) were fed over a three-week period with a commercial diet or one of seven casein-based diets. The latter were eithe r lipid-free or supplemented with 50-200 g linseed oil kg(-1) diet by dry w eight, 160 g linseed oil and 40 g 14:0 or 160 g linseed oil and 40 g 16:0. Three fish having filled guts were sampled from each dietary group and anal ysed for ultrastructural changes in the pyloric caecum. Increasing the dietary lipid level increased the accumulation of lipid drop lets in columnar absorptive enterocytes from about 9% of epithelial volume in fish fed a diet of 50 g linseed oil, to almost 61% in fish fed a diet of 200 g linseed oil. Replacing linseed oil in the diet with 14:0 (160 g lins eed oil + 40 g 14:0 kg(-1) diet) appeared to produce a smaller lipid loadin g (roughly 53%) but the difference was not statistically significant. Howev er, replacing 40 g linseed oil with 40 g of 16:0 in the diet decreased lipi d loading significantly to just under 10%. Epithelial damage to enterocytes was assessed using a ranking scale based on ultrastructural signs of cell and organelle swelling and degeneration. The extent of damage closely follo wed the level of lipid loading, being lowest in fish fed the lipid-free or low-lipid (damage index 0.07-0.13) diets, and highest in char maintained on a diet containing 200 g linseed oil (index 1.41). Replacing linseed oil wi th 14:0 (160 g linseed oil + 40 g 14:0) appeared to reduce the damage index to 0.77 but this was not significant. However, a significant reduction of the damage index to 0.27 was observed when linseed oil was replaced by 16:0 . We conclude that higher dietary linseed oil promotes lipid droplet accumula tion in enterocytes. The droplets are probably related to the amount of pol yunsaturated fatty acids in the lipid. Intracellular droplet formation and cellular damage are both reduced by adding saturated fatty acids to the die t. This could be related to disruptions in the lipoprotein assembly rate. T he cellular damages observed with high lipid diets are likely to be patholo gical and may lead to intestinal malfunction and represent a major infectio n route for pathogenic bacteria.