The animal model o f the uteroplacental insufficiency state described originally by Wigglesworth (4) has enabled investigators to study small for gestational age o r dysmature progeny with specific emphasis on glucose homeostasis. We have previously shown that 91 % of dysmature rat pups develop hypoglycemia 2-4 hr after birth and that prenatal glucocorticoid treatment significantly reduces this tendency (2). Our subsequent invcstigations have included an examination of the possible relationship between the protective effect of steroid hormones and the availability or utilization of gluconeogenic substrates.Pregnant Sprague-Dawley rats with accurately timed gestapriscd of fetally malnourished pups which were killed as soon as possible (within 1-5 min) after birth; blood from severed neck vessels for determination of plasma amino acid patterns was samplcd bcfore dcath. Group 2 (nutritionally deprived newborns) was comprised of dysmature pups which were maintained without nutritional support for 2-4 hr at an environmental temperature of 32". with sampling of blood carried out during this Interval. The weight of these animals was noted at birth and at the time of death. Experimental conditions for group 3 (glucocorticoid-treated animals) were as follows. The dams of these dysmature progeny received an intramuscular injection of 9-a- Mean values 2 SE are shown in micromoles per ml. IUGR = intrauterine growth retardation; GNG = gluconeogenic. P < 0.01, as compared to the untreated IUGR group of corresponding age.tions (within 12 hr) were utilized for this study. Under ether anesthesia, a low midline laparotomy was performed on the 17th-19th day after mating, and the appropriate surgical procedure was carried out as described in detail earlier (2); thus, vascular supply to one uterine horn was compromised with a ligature of silk suture (dysmature group), while the opposite horn was left intact, these animals serving as controls. At term (22 days of gestation), delivery by cesarian section was performed, and the rat pups were weighed immediately on a Mettler PT 1200 electronic balance. A reduction in weight of more than 15% compared to the mean of control littermates was considered evidence of intrauterine growth retardation (IUGR) on the ligated side. The experimental groups of rat pups with IUGR included the following. Grolrp I (newborns at birth) was comfluoroprenisolone acetate (1 mglkg) 24 and 4 8 hr before delivery; these small for gestational age animals o f g r o~r p 3 were then divided into two subgroups-one killed at birth, with sampling of blood as noted previously, and the other maintained under conditions of starvation similar to group 2, with blood sampling performed and the pups killed at 2-4 hr of age. Blood samples were collected in heparin-lithium fluoride tubes and were rapidly centrifuged. The plasma was then utilized for glucose and aminogram determinations using a Beckman E R A 2001 glucose analyzer and a Beckman 120M amino acid analyzer, respectively. Plasma amino acid profiles determined at birth...