Do low weight infants require nutrition with chain elongation-desaturation products of essential fatty acids?

Abstract

Little quantitative evidence is available to suggest if 22:4ω6, 22:5ω6, 22:5ω3 and 22:6ω3 are synthesized from 18:2ω6 and 18:3ω3 in the human fetus or if the fetus is dependent upon placental synthesis and transfer to obtain LCPE for synthesis of structural lipids. Therefore, the present study was initiated to determine developmental accretion of essential fatty acids in infant tissues during the last trimester through the early weeks of life. During the last trimester, brain levels of linoleic acids were low whereas substantial accretion of LCPE occurred. Postnatal brain development was characterized by an increase in brain linoleic acid content. Increase in chain elongation-desaturation products did not occur for several weeks postnatally. These results imply that LCPE are not synthesized at maximal rates for several weeks after birth suggesting that placental transfer of LCPE is of primary importance in accretion of these fatty acids in the fetus. Combined with analysis of early human milk these results support the need for use of human milk fats for nutrition of low birth weight infants as significant levels of LCPE precursors of prostaglandins and major brain structural fatty acids are present in milk lactated by mothers delivering low birth weight infants. The current study proposes an urgent need for developmental examination of fatty acyl-CoA elongating functions in infant tissues. Such in vitro verification of a requirement for LCPE would necessitate reevaluation of current nutrition practices for low birth weight infants.