NUTRITION DURING PREGNANCY, LACTATION, INFANCY, AND CHILDHOOD
Location: Children Nutrition Research Center (Houston, Tx)
Title: Protein kinetic differences between children with edematous and nonedematous severe childhood undernutrition in the fed and postabsorptive states
| Badaloo, Asha - UNIV WEST INDIES, JAMAICA |
| Reid, Marvin - UNIV WEST INDIES, JAMAICA |
| Forrester, Terrence - UNIV WEST INDIES, JAMAICA |
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 9, 2005
Publication Date: July 15, 2005
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2005. Protein kinetic differences between children with edematous and nonedematous severe childhood undernutrition in the fed and postabsorptive states. The American Journal of Clinical Nutrition. 82:792-800.
Interpretive Summary: There are two types of malnutrition, one in which the patient retains water in their bodies (edematous malnutrition) and one in which they do not (non-edematous). Those with edematous malnutrition are sicker and are more likely to die. The reasons that cause a malnourished child to develop the edematous form of the disease instead of the non-edematous form are not clear. It was hypothesized that inability to break down protein ,which is necessary to supply 20 compounds called amino acids for maintenance of important organ systems and functions, was one factor. To test this theory we measured protein breakdown rate in children with edematous and non-edematous malnutrition. We found that both in the fed and fasted state the children with edematous malnutrition broke down protein at a slower rate compared to children with non-edematous malnutrition. These findings indicate that a slower protein breakdown response to chronic food shortage may be the reason why some children develop edematous malnutrition.
BACKGROUND: Pathogenic factors that cause a child to develop the edematous instead of the nonedematous form of severe childhood undernutrition (SCU) during food deprivation are not clear. It was hypothesized that, in edematous but not nonedematous SCU, impaired protein breakdown leading to inadequate amino acids for maintenance of important organ systems was a factor. OBJECTIVE: We measured protein kinetics in children with edematous and nonedematous SCU. DESIGN: Endogenous leucine flux, an index of whole-body protein breakdown rate, was determined in 4 groups of children with edematous or nonedematous SCU in the malnourished and recovered states. Two groups were studied in the postabsorptive state, and 2 groups were studied in the fed state. RESULTS: In the postabsorptive state, leucine flux was slower (P < 0.01) in the edematous group than in the nonedematous group in the malnourished state, but in the recovered state, it was faster (P < 0.05) in the children who previously had edematous SCU. When compared with the malnourished state value, leucine flux at recovery doubled in the group that previously had edematous SCU, but it did not change in the other group. In the fed state, leucine flux was slower (P < 0.01) in the edematous group than in the nonedematous group in the malnourished state but not in the recovered state. In the recovered state, enteral leucine extraction by splanchnic tissues trended higher in the group that previously had edematous SCU than in the nonedematous group. CONCLUSION: These findings indicate different protein breakdown responses to food deprivation between children with edematous and nonedematous SCU and inherent differences in protein metabolism when they have recovered.