The aim of the present study was to obtain serial values of O 2 consumption (V O 2 ), CO 2 production (V CO 2 ) and energy expenditure (EE) in healthy but extremely-low-birth-weight infants (birth weight , 1000 g), during the first 5 weeks after birth. A total of seventeen spontaneously breathing and appropriate-for-gestational-age (birth weight and body length above the 10th and below the 90th percentile) preterm infants with gestational age 25 -28 weeks and birth weight 590-990 g were enrolled in the study. Calorimetry was performed using an open-circuit calorimeter on days 6, 12, 18, 24, 30 and 36 of postnatal life. During the 5 weeks of observation, V O 2 increased from 4·7 (SD 0·5) to 9·1 (SD 1·0) ml/kg per min, V CO 2 from 4·5 (SD 0·4) to 8·3 (SD 0·6) ml/kg per min and EE from 115 (SD 12) to 310 (SD 71) kJ/kg per d. The energy intake was always higher than EE, even at days 6 and 12. The RER decreased from 0·99 (SD 0·09) at day 12 to 0·91 (SD 0·05) at day 30. On all study days, there were highly significant positive correlations between energy intake and weight gain, EE and weight gain, and EE and energy intake (P,0·05). Multiple regression analysis showed that on most study days EE was more affected by energy intake than by weight gain. We conclude that in healthy preterm infants with birth weight , 1000 g, EE increases by about 150 % in the first 5 weeks after birth, and that the EE values are related to energy intake and weight gain independent of postnatal age. Energy expenditure: Growth: Preterm: Oxygen consumptionThe substantial improvement of the survival rate in extremely-low-birth-weight (ELBW) infants (birth weight , 1000 g) has changed the focus towards prevention of long-term morbidity. Adequate nutrition is an important prerequisite for intact survival of ELBW infants (Lucas, 1987;Lucas et al. 2001). Determinations of energy requirements are usually based on calculation of the energy balance (= energy intake (EI) -energy loss via faeces and urineenergy expenditure (EE)). Energy loss via faeces and urine is about 10 % EI, independent of postnatal age and EI in preterm infants (Sauer et al. 1984a). However, EE tends to increase with increasing age. Chessex et al. (1981) suggested that EE increases with age of preterm infants due to increasing EI. Their assumption was based on only three serial studies in preterm infants with a mean birth weight of 1155 (SD 39) g. Leitch & Denne (2000) summarised published EE values measured in seventy-five preterm infants with birth weight , 1000 g v. postnatal age, and found an increase of EE from 209 kJ/kg per d at birth to 272 kJ/kg per d at 5 weeks of age. However, thirty-five of the seventy-five infants were small-for-gestational-age with a mean postnatal age of 6·0 weeks, whereas forty infants had birth weights appropriate for gestational age and mean postnatal age of 2·5 weeks. Thus, the apparent increase in EE with age may be due in part to higher EE of small-for-gestational-age infants (Boehler et al. 1999).Recommendations for EI and dietary intakes are ...

Corticosteroids such as dexamethasone (DEX) increase leucine turnover and oxidation in humans and animals, indicating whole body protein catabolism. Recently, interest has been growing in the use of recombinant polypeptides such as GH and IGF-I in reversing various states of catabolism. The aim of our study was to investigate whether IGF-I reverses corticosteroid-induced protein catabolism in rapidly growing piglets. Also, we wanted to determine whether IGF-I attenuates corticosteroid-induced hyperglycemia. To study these questions, we performed leucine kinetic studies and measured blood glucose in eight piglets under postabsorptive conditions. We did three studies in each piglet: baseline, DEX treatment (5 mg/kg/d for 4 d), and DEX plus IGF-I treatment (25 micro g/kg/h for 6 h). DEX increased leucine turnover by 18 +/- 14% (mean +/- SD, p < 0.05), and oxidation by 132 +/- 64% (p < 0.01) over baseline values. Adding IGF-I to DEX treatment failed to reverse these changes in leucine kinetics. Turnover again increased by 18 +/- 8% (p < 0.01), and oxidation by 107 +/- 68% (p < 0.05) over baseline values. Nonoxidative leucine disposal, an indicator for protein synthesis, did not significantly differ after treatment with DEX or with DEX plus IGF-I. Blood glucose values increased over baseline values after DEX treatment, and approached baseline values after DEX plus IGF-I. We conclude that IGF-I attenuates corticosteroid-induced hyperglycemia, but does not reverse corticosteroid-induced protein catabolism in growing piglets.

Premature infants with low serum phosphate concentrations (<2 mmol/l) are at risk for osteopenia. Therefore, serum phosphate levels in premature infants should be kept above 2 mmol/l. Premature infants of 26-31 weeks gestational age (GA) have renal phosphate threshold concentrations (Tp/GFR) in the range of normal serum phosphate values (2 mmol/l). Therefore, these infants show significant urinary phosphate excretion only when serum phosphate levels are normal, and urinary phosphate excretion can be used to monitor phosphate supplementation. However, few data are available on extremely premature infants of 23-25 weeks GA. The objective of this study was to compare Tp/GFR levels in infants of 23-25 weeks GA to those in infants of 26-31 weeks GA. We retrospectively evaluated case notes of 12 infants of 23-25 weeks GA and compared them to 19 infants of 26-31 weeks GA. Tp/GFR was calculated from simultaneous measurements of urinary phosphate, urinary creatinine, serum phosphate, and serum creatinine. Tp/GFR values 3-5 weeks postnatally were lower in infants of 23-25 weeks GA (1.06+/-0.36 mmol/l, p<0.001) than in infants of 26-31 weeks GA (1.76+/-0.26 mmol/l). Near term (35-37 weeks postmenstrual age), there was no significant difference between Tp/GFR values in infants of 23-25 weeks GA (1.83+/-0.32 mmol/l) and in infants of 26-31 weeks GA (2.05+/-0.22 mmol/l). We conclude that at 3-5 weeks postnatally, infants of 23-25 weeks GA are at risk for low Tp/GFR values, leading to urinary phosphate excretion even in the presence of low serum phosphate levels. In these infants, serum phosphate levels should be monitored, and phosphate supplementation should be adjusted to keep serum phosphate levels above 2 mmol/l.

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