M. Reid, A. Badaloo, T. Forrester, W. Heird, F. Jahoor
{"title":"Response of splanchnic and whole-body leucine kinetics to treatment of children with edematous protein-energy malnutrition accompanied by infection.","authors":"M. Reid, A. Badaloo, T. Forrester, W. Heird, F. Jahoor","doi":"10.1093/AJCN/76.3.633","DOIUrl":null,"url":null,"abstract":"BACKGROUND\nAlthough 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.\n\n\nOBJECTIVE\nThe objective of this study was to determine whether the presence of infection alters the PEM-induced reduction in whole-body protein metabolism.\n\n\nDESIGN\nWe 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.\n\n\nRESULTS\nThe 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.\n\n\nCONCLUSIONS\nWhen 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.","PeriodicalId":315016,"journal":{"name":"The American journal of clinical nutrition","volume":"25 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"20","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The American journal of clinical nutrition","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/AJCN/76.3.633","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 20
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.