This study evaluated the arachidonic acid (AA) and docosahexaenoic acid (DHA) formation from d5-labeled linoleic acid (d5-LA) and ␣-linolenic acid (d5-LNA) precursors in infants with intrauterine growth restriction (IUGR) compared with control groups matched by gestational age (GA) or birth weight. We compared DHA and AA formation from deuterated precursors d5-LA and d5-LNA in 11 infants with IUGR with 13 and 25 control subjects who were appropriate for GA and matched by GA and by birth weight, respectively. After an enteral administration of d5-LA and d5-LNA, we determined unlabeled and d5-labeled fatty acids at 24, 48, and 96 h in plasma. Absolute concentrations and area under the curve (AUC) over the 96-h study were used for analysis. Absolute concentration of d5-DHA and the product/precursor ratio of the d5-labeled AUCs indicated a less active DHA formation from LNA in infants with IUGR compared with their GAmatched (2-fold) and birth weight-matched (3-fold) control subjects. The ratios of eicosapentaenoic and n-3 docosapentaenoic acid to DHA were also affected. Similar evaluation for the n-6 series was not significant. DHA metabolism is affected in infants with IUGR; the restricted DPA to DHA conversion step seems to be principally responsible for this finding. Abbreviations AA, arachidonic acid AGA, appropriate for gestational age AUC, area under the curve DHA, docosahexaenoic acid d5-LA, deuterated linoleic acid d5-LNA, deuterated ␣-linolenic acid DPA, docosapentaenoic acid EFA, essential fatty acids EPA, eicosapentaenoic acid GA, gestational age IUGR, intrauterine growth restriction LA, linoleic acid LCP, long-chain polyunsaturated fatty acids LNA, ␣-linolenic acid PGC-1, peroxisome proliferator-activated receptor-␥ coactivator-1 PPAR, peroxisome proliferator-activated receptor SGA, small for gestational age Intrauterine growth restriction (IUGR) is the result of the failure of the placenta to provide the necessary nutrients required by the fetus to maintain adequate growth (1). During the last trimester of gestation, there is a significant accumulation of long-chain polyunsaturated fatty acids (LCPs) in the fetus and an increase in the relative content of both n-6 and n-3 LCPs in the human brain and retina. Fetal tissue content of LCPs is dependent on maternal intake and on an adequate placental transfer. Thus, a greater risk for restricted in utero LCPs supply may occur in pregnancies that are complicated with abnormal placental function affecting nutrient transfer. Data derived from IUGR animal models indicate that placental insufficiency is associated with abnormalities in fetal lipid metabolism of skeletal muscle and liver (2,3). Cetin et al. (4) reported that fetuses with IUGR have a lower proportion of long-chain n-6 and n-3 fatty acids, arachidonic acid (AA), and docosahexae-