Insulin translocates adult glucose transporter - Glut 4 (insulin-responsive isoform) from an intracellular compartment to the plasma/sarcolemmal membrane causing an induction in glucose transport above basal. The fetus and newborn express relative insulin-resistance when compared to the adult due to lower Glut 4 levels. We hypothesized that in addition to low Glut 4 concentrations, insulin-induced translocation is also impaired in the fetus and newborn. To test this we intraperitoneally administered insulin or vehicle to the 20d fetus, 2d newborn, and adult rats, which led to a 5-fold increase in circulating insulin (p < 0.05) and a ≈50% decline in glucose levels (p< 0.05) at all ages. Using immunohistochemical analysis and semi-quantitation by computer based image analysis, we noted no insulin-induced change in the number of cells that demonstrate sarcolemmal association of Glut 4, or in the subcellular distribution of Glut 4 between the hindlimb skeletal myocytic intracellular and sarcolemmal compartments, in the fetus (n=3) and newborn (n=3) at 10, 20, 40, and 60 min. In contrast, the number of adult skeletal myocytes (n=3) that demonstrated a sarcolemmal association of Glut 4 did not change at 10 min, increased 5-fold at 20 min (p< 0.001), peaked at an 8-fold increase by 40 min (p < 0.001), followed by only a 2-fold increase at 60 min (p < 0.001). In these cells, insulin induced an increase in the sarcolemmal associated Glut 4 labeling from 30%(basal) to 70% (p < 0.001) at 10, 20, 40, and 60 min. Glut 1 in the basal and insulin treated states was observed in fetus and newborn sarcolemmal membranes and predominantly in the adult perineural sheaths with minimal myocytic sarcolemmal labeling. We conclude that insulin-induced Glut 4 translocation is not immunodetected in the fetus and newborn rat skeletal muscle within 60 min. We speculate that immaturity of the rat myocytic translocation machinery may contribute towards the fetus and newborn insulin resistance.