The effect of dietary lecithin and lipase, as a function of age, on n-9 fatty acid incorporation in the tissue lipids of Sparus aurata larvae

The present study tested the effect of dietary lecithin and exogenous lipase on the incorporation of oleic acid in the tissue lipids of gilthead seabream larvae (Sparus aurata). Two of four microdiets were prepared by the addition of [¹⁴C]oleic acid as free fatty acid (FFA) to diets containing either 5% cuttlefish liver oil (CLO) or 5% soybean lecithin. Glycerol tri[1-¹⁴C]oleate was similarly incorporated in two other diets identical in lipid (4% cuttlefish liver oil, 1% soybean lecithin) and non-lipid composition but differed in that one contained a supplement of 0.05% porcine lipase. The effect of these diets was tested by following the incorporation of the label (dpm/mg larvae DBW) in the neutral and phospholipid fractions of seabream larvae at four different ages (21, 27, 32 and 45 days after hatching). A significant (p<0.05) effect of dietary lecithin on the incorporation of labelled FFA in both larval neutral and phospholipid fractions was demonstrated at all ages. This was particularly pronounced during early development (day 21) where fish fed the lecithin supplement incorporated 6.75 times more label than the diet containing [¹⁴C]oleic acid in CLO. The dietary lecithin enhancing effect diminished with age but was still significant at day 45 (2.17 times more label). In addition, the label was considerably higher in the phospholipid fraction compared to the neutral lipid, reflecting the high demand for membrane synthesis during rapid growth. Lecithin fed larvae demonstrated a higher consumption rate and efficiency of incorporation than fish consuming the cuttlefish liver oil diet, suggesting an emulsifying function for dietary phospholipid. In contrast, the supplementation with lipase showed a clear effect only in older fish where 45 day old larvae fed the lipase diet demonstrated a 3.42 times increase in radioactivity in their tissue lipids. This late lipase response may be the result of an insufficient level of dietary lecithin (M) and a short intestinal length being ineffective, in the early larval stages, in incorporating labelled free fatty acid from dietary glycerol tri[1-¹⁴C]oleate breakdown.