Uteroplacental insufficiency leading to IUGR is associated with an increased risk for the development of insulin resistance and NIDDM. Because increased lipid oxidation is associated with insulin resistance, we hypothesized that gene expression of mitochondrial enzymes involved in fatty acid oxidation would be altered in muscle of IUGR juvenile rats. We performed bilateral uterine artery ligation to induce IUGR and sham surgery (C) in pregnant rats on day 19 of gestation. Muscle was harvested on day 14(J14) and day 21(J21) of neonatal life. Using RT-PCR with an internal control, we measured mRNA levels of carnitine palmitoyl-transferase II (CPTII)(transports fatty acids across the inner mitochondrial membrane), L3HD (a component of the beta-oxidation complex), electron transfer flavoprotein (ETF)(a soluble matrix protein which participates in transfer of electrons to the respiratory chain at complex II), and succinate dehydrogenase (SD) (a component of complex II). Gene expression of all four enzymes were not significantly different in IUGR J14 muscle (C=1.0, CPTII=1.03, L3HD=0.95, ETF=0.74, SD=1.1). In J21 muscle, gene expression of CPTII, ETF, and SD were not significantly altered in IUGR muscle; however, in contrast, gene expression of L3HD was increased almost two fold (C=1.0, CPTII=1.24, L3AD=1.94*, ETF-1.08, SD=1.12; *p<0.05). L3HD is a unique component of the beta oxidation enzyme complex because it alone competes with three NAD-dependent dehydrogenases of the Krebs cycle. As a result, L3HD may play an important role in determining the dynamic balance between glucose and lipid oxidation. Our findings are consistent with our previous observation of an increased mitochondrial NADH/NAD ratio in J21 IUGR muscle which also favors beta oxidation. We conclude that the altered metabolic milieu associated with IUGR leads to increased gene expression of L3HD. We speculate that the phenomena of metabolic imprinting may eventually lead to the development of insulin resistance in IUGR offspring.