Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer reviewed journal
Publication Acceptance Date: 3/15/2006
Publication Date: 7/15/2006
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2006. Glycine production in severe childhood undernutrition. American Journal of Clinical Nutrition. 84:143-149. Interpretive Summary: The compounds used to make proteins in our bodies are called amino acids. Some amino acids cannot be made in our body and have to be provided by our food. These are the nutritionally essential amino acids. Others are called nutritionally non-essential amino acids because they are obtained from our diet, plus they can be made by our body. One such amino acid is glycine which is needed in large quantities to make numerous proteins and several other compounds that are necessary to support life. It is not known, however, whether the child who has severe childhood undernutrition (SCU) is capable of making enough glycine to compensate for the smaller amount coming from the chronic deficiency in food intake. We therefore measured the amount of glycine produced by children with SCU. We found that children with SCU were making the same amount of glycine as when they were recovered from their undernutrition and had become healthy. These findings suggest that children with SCU can increase the amount of glycine they are making to compensate for the reduced contribution from chronic food deprivation.
Technical Abstract: BACKGROUND: Although nutritionally dispensable amino acids are not essential in the diet, from a biochemical standpoint, dispensable amino acids such as glycine are essential for life. This is especially true under unique circumstances, such as when the availability of labile nitrogen for dispensable amino acid synthesis is reduced, as in severe childhood undernutrition. OBJECTIVE: We aimed to measure glycine production in children with edematous and nonedematous severe childhood undernutrition. DESIGN: Glycine flux and splanchnic glycine extraction were measured in 2 groups of children with edematous (n = 8) and nonedematous (n = 9) severe childhood undernutrition when they were infected and malnourished (clinical phase 1), when they were still severely malnourished but no longer infected (clinical phase 2), and when they were recovered (clinical phase 3). RESULTS: Total and endogenous glycine flux and splanchnic glycine uptake did not differ significantly between the edematous and nonedematous groups during any clinical phase. In both groups of subjects, none of the glycine kinetic parameters changed significantly from clinical phase 1 through phases 2 and 3. Compared with the value at clinical phase 3, plasma glycine concentrations were not significantly lower during clinical phase 1 or 2 in either group. CONCLUSIONS: These findings suggest that children with severe childhood undernutrition can increase their de novo glycine synthesis to compensate for the reduced contribution from chronic food deprivation. The maintenance of the plasma glycine concentration suggests that the rate of glycine production was sufficient to satisfy metabolic demands in these children when they were acutely undernourished and infected.