Whole-body protein turnover in preterm appropriate for gestational age and small for gestational age infants: comparison of [15N]glycine and [1-(13)C]leucine administered simultaneously.
ABSTRACT Measurements of whole-body protein turnover in preterm infants have been made using different stable isotope methods. Large variation in results has been found, which could be due to different clinical conditions and/or the use of different tracers. We studied 14 appropriate for gestational age and nine small for gestational age orally fed preterm infants using [15N]glycine and [1-(13)C]leucine simultaneously, which allowed us to make a comparison of commonly used methods to calculate whole-body protein turnover. Whole-body protein turnover was calculated from 15N enrichment in urinary ammonia and urea after [15N]-glycine administration and from the 13C enrichment in expired CO2 after administration of [1-(13)C]leucine. Enrichment of alpha-ketoisocaproic acid after [1-(13)C]leucine constant infusion was measured as a direct parameter of whole-body protein turnover. Group means for whole-body protein turnover using [15N]glycine or [1-(13)C]leucine ranged from 10 to 14 g.kg-1.d-1, except when using the end product method that assumes a correlation between leucine oxidation and total nitrogen excretion. We found very low 15N enrichment of urinary urea in the majority of small for gestational age infants. These infants also had a lower nitrogen excretion in urine and oxidized less leucine. Nitrogen balance was higher in small for gestational age infants (416 +/- 25 mg.kg-1.d-1) compared with appropriate for gestational age infants (374 +/- 41 mg.kg-1.d-1, p = 0.003). [15N]Glycine does not seem to exchange its label with the body nitrogen pool to a significant degree and is therefore not always suitable as a carrier for 15N in protein turnover studies in premature infants.
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ABSTRACT: Changes in parenteral nutrition of the term and preterm newborns There is an increase in survival rates of very low birth weight infants in recent years. The rise in survival of very low birth weight infants is associated with increased use of parenteral nutrition and change of practice in parenteral nutrition, since very low birth weight infants can not be fed ente- rally in early period of life. Until recently, it was also common practice to initiate an aminoacid in- fusion at 0.5 g/kg/day between 24 and 48 hours of life and then to initiate a lipid emulsion at 0.5 g/kg/day 24 hours later. Both infusions would then be increased by 0.5 g/kg/day increments to 3- 3.5 g/kg/day. Reports that an aminoacid infusion providing at least 1.5 g/kg/day of protein is requ- ired to achieve a positive protein balance, have resulted in recommendations that at least 1.5 g/kg/day of protein should be started within the first 24 hours after birth and then increased to 3.5- 4 g/kg/day by 0.5-1 g/kg/day increments. Early aggressive nutrition is a new concept which means initiation of an aminoacid infusion providing about 3 g/kg/day within hours of birth, initiation of a lipid emulsion of 0.5-1 g lipid/kg/day within 24-30 hours of birth, with subsequent increases pro- viding up to 3.5-4 g protein/kg/day and 2-3 g lipid/kg/day for the following days. A daily energy in- take should be 120-130 kcal/kg/day in healthy preterm neonates and 100-120 kcal/kg/day in he- althy term neonates. Aim of this strategy is to provide nutrient intakes that permit the rate of post- natal growth and the composition of weight gain to approximate that of a normal fetus of the sa- me postmentruel age.
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ABSTRACT: Mutations in the methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome, a severe neurodevelopmental disease associated with ataxia and other post-natal symptoms similar to autism. Much research interest has focussed on the implications of MeCP2 in disease and neuron physiology. However, little or no attention has been paid to how MeCP2 turnover is regulated. The post-translational control of MeCP2 is of critical importance, especially as subtle increases or decreases in MeCP2 amounts can affect neuron morphology and function. The latter point is of particular importance for gene therapeutic approaches in which exogenous wild-type MeCP2 is being introduced into diseased neurons. Further to this, we propose two hypotheses. The first hypothesis discusses the poly-ubiquitin-mediated post-translational regulation of MeCP2 through its two PEST domains. The second hypothesis explores the use of histone deacetylase inhibitors to modulate the amounts of MeCP2 expressed in conjunction with the aforementioned therapeutic approaches.BioEssays 04/2009; 31(5):561-9. · 5.42 Impact Factor
Article: Nutrition en période néonataleArchives De Pediatrie - ARCHIVES PEDIATRIE. 01/1996; 3.