MODIFICATION OF MILK FORMULA TO ENHANCE ACCRETION OF LONG-CHAIN N-6 AND N-3 POLYUNSATURATED FATTY-ACIDS IN ARTIFICIALLY REARED INFANT RATS

Artificially reared infant rats were used to determine the effects of long-chain polyunsaturated fatty acid (LCPUFA) supplementation on bloo d and tissue concentrations of arachidonic acid (AA) and docosahexaeno ic acid (DHA). Beginning at 7 d of age, infant rats were fed for 10 d with rat milk formulas supplemented with AA at 0, 0.5 and 1.0%, or sup plemented with DHA at 0, 0.5 and 1.0% of total fatty acid. The supplem entation of AA increased accretion of the fatty acid in tissue and blo od phospholipids with a maximum increase of 9% in brain, 15% in liver, 25% in erythrocytes, and 43% in plasma above the values of unsuppleme nted infant rats. Rat milk formula containing 1.0% of AA had no added benefits over that containing 0.5% of AA. The supplementation of DHA i ncreased phospholipid DHA by a maximum of 24% in brain, 87% in liver, 54% in erythrocytes, and 360% in plasma above the unsupplemented contr ol. The increase in tissue and blood DHA was concentration-dependent o n formula fatty acid. Brain phosphatidylcholine and phosphatidylethano lamine were similarly enriched with AA and DHA by supplementation of t he corresponding fatty acids. In general the observed increase of AA w as accompanied by a decrease in 16:0, 18:1n-9, and/or 18:2n-6, whereas the increased DHA was associated with a reduction of 18:1n-9, 18:2n-6 , and/or 20:4n-6. Clearly, infant rats were more responsive to DHA tha n AA supplementation, suggesting a great potential of dietary manipula tion to alter tissue DHA concentrations. However, the supplementation of DHA significantly decreased tissue and blood AA/DHA ratios (wt%/wt% ), whereas there was little or no change in the ratio by AA supplement ation. Although the physiological implications of the levels of AA and DHA, and AA/DHA ratios achieved under the present experimental condit ions are not readily known, the findings suggest that artificial reari ng could provide a suitable model to investigate LCPUFA requirements u sing various sources of AA and DHA in rats.