To establish nutritional management of low birth-weight infants according to their individual metabolic situation, hepatocellular partial function was studied in 13 appropriate (AGA) and 11 small-for-gestational-age (SGA) low birthweight (LBW) infants during the first weeks of postnatal life. The concentrations of total bile acids and of alpha-amino-nitrogen in serum, the renal excretion of urea and ammonia and the renal excretion of 15N after enteral administration of 3 mg 15N-labeled methacetin/kg were measured. In comparison to AGA infants, SGA infants had elevated serum concentrations of total bile acids and of alpha-amino-nitrogen, decreased excretion of urea, increased excretion of ammonia in urine, and lower urinary 15N-excretion after enteral administration of 15N-labeled methacetin. The data suggest that hepatocellular functions are influenced by intrauterine growth retardation resulting in a reduced metabolic capacity in SGA infants. The metabolic differences between SGA and AGA infants should be considered in the nutritional management of LBW infants.

The urea-synthesizing capacity of the liver was studied in 20 healthy preterm infants during the first month of life. The urea-synthesizing capacity was estimated by the ratio of ¹⁵N abundances of ammonia and urea in the 6-hour urine after administration of 3 mg ¹⁵N-labelled ammonium chloride/kg body weight. The ratio increases with increasing protein intakes from the 2nd to the 3rd week of life. On protein intakes of more than 3 g/kg/ day from the 3rd week to the end of the 2nd month of life, the ratio decreases suggesting a maturation of the urea cycle during the first weeks of life.

The influences of the gestational age (range: 28-36 weeks) and the postnatal age (range: 6–100 days) on the biotransformation capacity of the liver were studied in 51 preterm appropriate-for-gestational-age infants and in 20 preterm small-for-gestational-age infants using the [¹⁵N]methacetin urine test. Methacetin is a test drug assessing a two-step pathway of biotransformation including monooxygenation and conjugation. After oral administration of 3 mg [¹⁵N]methacetin/kg body-weight, the cumulative ¹⁵N excretion in urine during the consecutive 9 h was measured and used as a marker of microsomal biotransformation capacity. In preterm appropriate-for-gestational-age infants, the biotransformation capacity increases with gestational age as well as with postnatal age, but the strongest correlation could be found between cumulative [¹⁵N] excretion and postmenstrual age. Intrauterine growth retardation results in lower biotransformation capacity (26.3 ± 11.3 vs. 36.1 ± 9.6% [¹⁵N] excretion, expressed as percentage of intake) and disturbed postnatal development of this hepatic function. The data indicate that normal intrauterine development is a prerequisite for normal postnatal development of the biotransformation capacity, which might have consequences for the metabolism and efficacy of certain drugs in small-for-gestational-age infants.

In this mouse model, oral vaccination with RotaTeq and Rotarix prevented most RRV-induced BA. This provides a new approach to a better understanding of both the pathomechanism of BA development and the capabilities of the innate immune system. It also suggests a first approach for prophylaxis against BA.

The postnatal development of the urea-synthesizing capacity was studied in 21 preterm infants with intrauterine growth retardation (IUGR) and compared with results found in 12 infants without IUGR as controls. The urea-synthesizing capacity was estimated by the ratio Q of ¹⁵N abundance of ammonia and urea in 6-hour urine samples collected after enteral administration of 3 mg [¹⁵N]H₄Cl/kg body weight. The measurements were performed on the first day when a protein intake of 3.0–3.5 g/kg/day and an energy intake of 120 kcal/kg/day were tolerated (study day 1: postnatal 14–21 days) and on the day of discharge from the hospital (study day 2: postnatal age 39–56 days). The group of infants with IUGR was subdivided in one group of infants who developed catch-up growth (n = 12) and one group who did not demonstrate catch-up growth (n = 9). On study day 1, the Q values of the IUGR infants without catch-up growth were significantly higher than those of the IUGR infants with catch-up growth (13.4 ± 2.3 vs. 9.2 ± 2.2) or of the control infants without IUGR. During the time period from study day 1 to study day 2 the Q values of the IUGR infants with catch-up growth decreased significantly (9.2 ± 2.2 vs. 4.8 ± 2.0; p < 0.001) and were in the range of the control infants without IUGR. In contrast, the Q values of the IUGR infants without catch-up growth did not significantly change during the study period (13.4 ± 2.3 vs. 11.3 ± 2.8; p = 0.097). On both study days there was a significant correlation between the Q values and the degree of IUGR (study day 1: r = 0.652, p < 0.01; study day 2: r = 0.842, p < 0.001). The data indicate that the urea-synthesizing capacity of preterm infants increases during early postnatal life and that severe IUGR may impair this development. Metabolic investigations using urea as marker for evaluation of optimal quantity or quality of dietary proteins should carefully be interpreted when infants with severe IUGR are studied.