Conversion of alpha-linolenate to docosahexaenoate is not depressed by high dietary levels of linoleate in young rats: tracer evidence using high precision mass spectrometry.

The conversion of alpha-linolenate (18:3n-3) to docosahexaenoate (22:6n-3) in the presence of low and high dietary levels of linoleate (18:2n-6) is reported in young rats using [U-13C]-alpha-linolenic acid (18:2n-3*) and high precision gas chromatography-combustion isotope ratio mass spectrometry (GCC-IRMS). After consuming an 18:3n-3-deficient diet for 4 weeks, dams were bred and assigned to one of three diet groups: a) 2 g 18:3n-3/kg diet and 17 g 18:2n-6/kg diet (Lo-18:2), b) 2 g 18:3n-3/kg diet and 140 g 18:2n-6/kg diet (Hi-18:2), or c) essential fatty acid-deficient diet (EFAD). Pups were weaned to the maternal diets. At 42 days of age, pups were gavaged with 1 mg 18:3n-3*, and killed 48 h later. Fatty acid composition of liver reflected the diets to a greater extent than did the brain, and 22:5n-6 replaced 22:6n-3 in the brain. About 80% of the label in liver, brain, and plasma was found as 22:6n-3* for the replete groups. The enrichment pattern was similar in liver and plasma except for 18:3n-3, which was higher in liver. Total label detected was 4-fold higher in the EFAD livers and 2-fold higher in the EFAD brains than in the other groups, which were indistinguishable. Conversion of 18:3n-3* to 22:6n-3* was greater in livers from the Hi-18:2 group than from the Lo-18:2 group (P < 0.05). Estimates of overall label recovery in liver and brain were consistent with literature values. These data indicate that high dietary levels of 18:2n-6 do not inhibit conversion of a single dose of 18:3n-3 to 22:6n-3 in young rats, and demonstrate the applicability of high precision GCC-IRMS to fatty acid tracer studies.