Rats rendered asymmetrically growth retarded in utero do not grow to their full genetic potential postnatally. The mechanisms responsible for this phenomenon are unknown but may involve decreased cell glucose transport. Previous studies have shown that IGF-I increases body weight in normal neonatal rats (Philipps 1988). IGF-I also induces Glut 1 expression in muscle of normal fetal rats (Simmons 1993). We administered IGF-I to SGA rats during the neonatal period to determine whether exogenous IGF-I may correct impaired growth and affect cell glucose transport. Pregnant rats had both uterine arteries ligated on day 19 of gestation (term=21.5 days). Litters from sham operated mothers served as controls. Dams delivered spontaneously and litters were reduced to 4 on day 1. Pups received twice daily injections of IGF-I (15μg/day) or saline from day 4 to 15. Four groups of pups were studied: SGA:IGF-I injected; SGA:saline injected; sham:IGF-I injected; sham:saline injected. Muscle tissue was harvested from day 15 pups and protein and RNA extracted. Polymerase chain reaction (PCR) amplification and quantification by phosphorimaging, and Western and Northern blot analyses were performed. On days 1-15 saline and IGF-I SGAs weighed significantly less than saline and IGF-I shams (p<0.05). IGF-I did not affect SGA growth, whereas IGF-treated shams showed accelerated growth by day 11 (p<0.05). Glut 1 and Glut 4 mRNA and protein levels were significantly less in saline SGAs versus saline shams(Glut 1: 45%, 50% of saline shams; Glut 4: 30%, 45% of saline shams)(p<0.05). IGF-I did not increase Glut 1 and Glut 4 mRNA and protein in IGF-I SGAs compared to saline SGAs. However, in IGF-I shams, muscle Glut 1 mRNA and protein were increased 45% and 65% compared to saline shams(p<0.05). Glut 4 mRNA and protein levels were likewise significantly elevated in IGF-I shams v saline shams (65%, 54%) (p<0.05). We conclude that IGF-I was unable to normalize poor postnatal growth or stimulate Glut expression in the SGA rat however, IGF-I does stimulate growth and Gluts 1 and 4 in muscle of normal rats. The inability of IGF-I to stimulate growth in the SGA rat may in part be due to a lack of response of muscle Gluts to IGF-I.