Alterations in the maternal endocrine, nutritional and metabolic environment disrupt the developmental trajectory of the fetus leading to adulthood diseases. Female offspring of rats, subhuman primates and sheep treated prenatally with testosterone (T) develop reproductive/metabolic defects during adult life that are similar to those which occur after intrauterine growth retardation. In the present study we determined if prenatal T treatment produces growth retarded offspring. Cottonseed oil (C) or T-propionate (100 mg im) was administered twice weekly to pregnant sheep between 30 to 90 days of gestation (term is 147 days) (C: n = 16; prenatal T: n = 32). Newborn weight and body dimensions were measured the day after birth and postnatal weight gain monitored for 4 months in all females and a subset of males. Consistent with its action, prenatal T treatment produced females and males with greater anogenital distances relative to controls. Prenatal T treatment reduced body weights and heights of newborns from both sexes and chest circumference of females. Prenatally T-treated females but not males exhibited catch-up growth during 2-4 months of postnatal life. Plasma IGFBP-1 and IGFBP-2 but not IGF-I levels of prenatally T-treated females were elevated the first month of life, a period when the prenatally T-treated females were not exhibiting catch-up growth. This is suggestive of reduced IGF availability and potential contribution to growth retardation. These findings support the concept that fetal growth retardation and postnatal catch-up growth, early markers of future adult diseases, can also be programed by prenatal exposure to excess sex steroids.