Interaction of n‐3 long‐chain polyunsaturated fatty acids with n‐6 fatty acids in suckled rat pups

Abstract

The addition of long-chain polyunsaturated fatty acids (LCP: C20, and C22) to infant formula may permit fatty acid accretion rates similar to breast-fed infants, and may have long-term outcome benefits, such as improved visual acuity and cognitive development. Although fish oil may provide a source of n-3 LCP, sources of n-6 LCP have been more difficult to identify. The present study evaluates the effects of n-3 and n-6 LCP derived from single-cell oils on liver, plasma, and brain fatty acid levels in a neonatal animal model. Newborn rat pups were suckled for 14 d by dams receiving diets containing n-3 LCP alone or combinations of n-3 LCP and increasing doses of linoleic acid (18:2n-6) or arachidonic acid (20:4n-6). Dietary groups received 2% n-3 LCP and 1, 2, or 5% of either 18:2n-6 or 20:4n-6. The 20:4n-6 source also contained modest levels of 18:2n-6. At the termination of the study, liver, plasma, and brain were obtained from the rat pups and the phospholipid fatty acid profiles determined. The results indicate complex interactions of n-3 and n-6 fatty acids. Groups receiving dietary 20:4n-6 incorporated higher levels of n-6 LCP into tissues than did the groups receiving 18:2n-6. The brain was relatively resistant to changes in fatty acid composition compared with the liver and plasma. As expected, tissue n-3 LCP levels were reciprocally related to n-6 levels. The present results document that single-cell LCP oils are bioavailable in a neonatal animal model. The use of 20:4n-6 is a more effective means of supporting n-6 status than the use of 18:2n-6. These results may have implications for the addition of LCP to infant formula.

Lowering dietary n-6 polyunsaturated fatty acids

“…Five studies reported higher brain DHA in the low linoleic acid groups [31,32,35,37,39], whereas seven showed no effect of varying linoleic acid on brain DHA [33,34,36,38,[40][41][42]. The five studies that reported an effect all had dietary linoleic acid levels in the higher group of over 30% of fatty acids, whereas five of the seven showing no effect had dietary linoleic acid levels of less than 30% in the high group.…”

“…Twelve studies were identified that examined the effect of varying concentrations of dietary linoleic acid during early life on brain ARA and DHA [31][32][33][34][35][36][37][38][39][40][41][42]. Early life studies are here defined as those in which the dietary intervention began before weaning; in six studies dams were fed the diets throughout pregnancy [31][32][33][34][35][36], in two the dams were put on the diets in the second half of pregnancy [37,38], and in four, piglets were hand fed liquid diets from birth [39][40][41][42] (Table 1a).…”

“…Early life studies are here defined as those in which the dietary intervention began before weaning; in six studies dams were fed the diets throughout pregnancy [31][32][33][34][35][36], in two the dams were put on the diets in the second half of pregnancy [37,38], and in four, piglets were hand fed liquid diets from birth [39][40][41][42] (Table 1a). Seven of the 12 studies reported lower brain ARA in the low linoleic acid groups [37][38][39][40][41], whereas five studies detected no change in ARA [32][33][34]. The mean percentage of dietary fatty acids as linoleic acid in the studies finding no effect was 5.8% in the low group and 27% in the high group, whereas in the studies reporting an effect, linoleic acid accounted for on average 7% of dietary fatty acids in the low group and 37% in the higher groups.…”

“…Seven studies were identified that measured brain concentrations of ARA and DHA following feeding of different levels of ARA during early life [33,34,[56][57][58][59][60] (Table 2a).…”

The effects of dietary α‐linolenic acid compared with docosahexaenoic acid on brain, retina, liver, and heart in the guinea pig

“…Whether the increased blood DHA and AA levels are reflected in tissues such as retina and brain is not known. For example, it has been reported that rats fed dietary AA supplements show significant increases in the plasma level of AA but not in the brain (14). Clearly, such issues can only be addressed easily with animal studies.…”