|Reid, Marvin - BAYLOR COLLEGE OF MED|
|Badaloo, Asha - U WEST INDIES, JAMAICA|
|Forrester, Terrence - U WEST INDIES, JAMAICA|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 26, 2001
Publication Date: September 20, 2002
Citation: REID, M., BADALOO, A., FORRESTER, T., HEIRD, W.C., JAHOOR, F. 2002. RESPONSE OF SPLANCHNIC AND WHOLE-BODY LEUCINE KINETICS TO TREATMENT OF CHILDREN WITH EDEMATOUS PROTEIN-ENERGY MALNUTRITION ACCOMPANIED BY INFECTION. AMERICAN JOURNAL OF CLINICAL NUTRITION. 76:633-640. Interpretive Summary: When young children become severely malnourished the proteins of their bodies are broken down and excreted at a slower rate. This adaptation helps to slow down the rate at which they lose their lean tissues and organ proteins. On the other hand when children become infected with a virus or bacteria the proteins of their bodies are broken down and excreted at a faster rate and they lose lean tissues and organ proteins very quickly. Most malnourished children also become infected and at present it is not known whether the sparing of body proteins by malnutrition is affected by the response to an infection. In this study we determined whether the presence of infection alters the reduction in whole body protein metabolism brought on by malnutrition in children who were both malnourished and infected. We found that severe malnutrition induces a marked reduction in whole body protein synthesis and breakdown rates and that the presence of infection does not alter this adaptation.
Technical Abstract: BACKGROUND: Although the reduction in whole-body protein turnover and net protein loss induced by protein-energy malnutrition (PEM) has been well documented, it is unclear whether the protein-sparing mechanisms elicited by chronically inadequate intakes of dietary protein and energy are affected by the protein catabolic response to infection. OBJECTIVE: The objective of this study was to determine whether the presence of infection alters the PEM-induced reduction in whole-body protein metabolism. DESIGN: We determined whole-body leucine kinetics in 4 boys and 3 girls aged 6-15 mo with edematous PEM and infection approximately 3 d after admission (study 1), when they were both infected and malnourished; approximately 11 d after admission (study 2), when infection had resolved but they were still anthropometrically malnourished; and at recovery (study 3), when weight-for-length was at least 90% of that expected. RESULTS: The children had significantly less leucine flux in both study 1 and study 2 than they had in study 3. There were no significant differences in the amount of leucine released from protein breakdown or used for protein synthesis between study 1 and study 2. There were no significant differences in leucine balance or in either the amount or percentage of enteral leucine extracted by the splanchnic tissues among the 3 studies. CONCLUSIONS: When subjects are in the fed state, severe PEM induces a marked reduction in whole-body protein synthesis and breakdown rates, and the presence of infection does not alter this adaptation and hence the overall protein balance. A corollary is that children with severe PEM do not mount a protein catabolic response to infection.