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Growth and nitrogen and energy balances were studied with a combined technique of nutrient balance and indirect calorimetry measurement in two groups of eight very low birth weight infants fed pooled pasteurized human milk (HM) or cow's milk casein hydrolysate supplemented HM (HM-Pr). There was no difference in the amount of energy absorbed (91 ± 17 kcal/kg/day with HM-Pr versus 95 ± 8 with HM-P) or in the growth rate. The infants fed HM-Pr had a higher nitrogen intake (602 ± 80 versus 395 ± 64 mg/kg/day; p<0.001), urinary nitrogen excretion (160 ± 64 versus 78 ± 16 mg/kg/day; p<0.005) and nitrogen retention (326 ± 32 versus 252 ± 48 mg/kg/day; p<0.01). They also had increased plasma concentrations of essential amino acids, urea nitrogen, and total protein without metabolic imbalance. Energy expenditure was higher (58 versus 49 kcal/kg/day; p<0.005) and energy storage lower (33 versus 47 kcal/kg/day; p<0.05) with HM-Pr. In percent of weight gain, protein and fat accretion represented 12 and 14 in HM-Pr group versus 10 and 27 in HM group. Very low birth weight infants fed casein hydrolysate supplemented pooled HM achieved a growth rate and a weight gain composition similar to the fetus. (Pediatr Res 21 458-461,1987)

ABSTRACT: As the fate of glucose and lipids infused during total parenteral nutrition is not well known in infants, we assessed energy substrate oxidation in 36 patients (mean age: 5.8 ± 3.6 mo) on continuous total parenteral nutrition. The infants received isocaloric feeding regimens with nonprotein energy intakes either based on glucose alone (group 1) or on glucose-lipid mixtures providing 15% (group 2), 35% (group 3), 50% (group 4), or 70% (group 5) energy as fat for at least 6 d before glucose and fat oxidation rates were measured by open-circuit indirect calorimetry. Oxidative glucose disposal reached a maximal rate of 12.6 ± 1.2 mg/kg·min (17.9 ± 1.7 g/kg·d) in patients with the higher glucose infusion rates. Glucose infused in excess of maximal oxidative disposal was stored, mainly as fat. The increase in glucose infusion rate was paralleled by an increase in energy expenditure amounting to 16% of the energy value of infused glucose. Net fat oxidation was only observed in group 3 (1.6 ± 0.7 g/kg·d), 4 (3.4 ± 0.6 g/kg·d), and 5 (3.9 ± 0.4 g/kg·d) patients, with glucose infusion rates lower than 18.3 g/kg·d. However, there was no further increase in fat oxidation in group 5 as compared to group 4 patients, despite a further increase in fat intake, which only resulted in increasing fat deposition. Thus, fat infusion aiming at a significant contribution to coverage of energy expenditure requires that glucose oxidation be equal to or lower than maximal oxidative glucose disposal, hence that glucose infusion rates be lower than 18 g/kg·d. In these conditions, excessive fat deposition may be prevented by adapting fat infusion to fat oxidation capacity, which did not exceed 4 g/kg·d in our patients.

Perinatal metabolism of vitamin D was studied in premature babies with the aim of: (1) reporting the relationship between the pregnant mother and her preterm infant and the metabolism of vitamin D during the first weeks of life, and (2) assessing the effect of vitamin D metabolites on phosphorus calcium and magnesium intestinal absorption. There was only a positive correlation between plasma cord calcium and 25-hydroxyvitamin D levels and the mother’s plasma levels at birth. During the hypocalcemic episode observed during the first week of life, vitamin D activation did occur, but later on rickets or osteomalacia cannot be due to the low levels of vitamin D metabolites in the preterm receiving an adequate dose of vitamin D (1,000–1,200 IU of D2). Calcitriol, the major metabolite of vitamin D, is acting on the intestine and promotes calcium absorption even in very tiny prematures. The pathogenesis of hypomineralization in the preterm infant is due to the low intake of calcium or phosphorus and/or poor absorption of calcium in the case of vitamin D deficiency.

Weight gain composition of growing very low birthweight (VLBW) premature infants can be assessed by a combined technique of nutrient balance and indirect calorimetry measurement. Both protein and energy intakes play an important role in the rate of growth and in the amount of non-protein energy (i.e. fat) storage. High energy intake is not always correlated with a higher rate of growth and can lead to high fat storage.

In order to evaluate tissue taurine storage during pregnancy, we determined the taurine concentration of a skeletal muscle (abdominal wall), the brain (left parietal lobe), and the liver (right lobe) in 41 children aged 1–10 days, born after 24–41 weeks gestation. Samples were obtained during autopsy. Taurine dosage was carried out by gas chromatography. Muscle and liver taurine concentrations decreased with the duration of gestation. For a given duration of pregnancy, there was no correlation between birth weight and these three tissue concentrations. From these results, we estimate that the fetus accumulates 35–40 μmol/24 h of taurine during the last 3 months of gestation.

In order to determine whether the decrease in taurine concentration in the placenta during pregnancy could affect fetal development, as has been observed in animals, we measured the concentration of taurine in placentas obtained after vaginal expulsion. 31 placentas from women with normal pregnancies of over 37 weeks who have given birth to infants of normal weight (3,200 ± 310 g) were included in the study. In addition, 26 placentas of infants considered to be hypotrophic were also included (gestation over 37 weeks, birth weight: 2,260 ± 230 g). The taurine was assayed using gaz-liquid chromatography. The concentration of taurine in the placenta was 2.80 ± 0.56 μmol/g for the placentas of normal birth weight infants and 2.40 ± 0.64 μmol/g for the placentas of hypotropic infants (p < 0.02). There is no significant correlation in normal and hypotrophic newborns between the gestation period, the weight and height at birth, the weight of the placenta, and the taurine concentration in the placenta. The taurine concentration in placentas of hypotrophic born infants is significantly reduced compared to the placentas from normal infants.