Sulfur amino acid metabolism in children with severe childhood undernutrition: methionine kinetics

Authors: Jahoor, Farook; BADALOO, ASHA - UNIVERSITY OF WEST INDIES; REID, MARVIN - UNIVERSITY OF WEST INDIES; FORRESTER, TERRENCE - UNIVERSITY OF WEST INDIES

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/20/2006
Publication Date: 12/14/2006
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2006. Sulfur amino acid metabolism in children with severe childhood undernutrition: Methionine kinetics. American Journal of Clinical Nutrition. 84(6):1400-1405.

Interpretive Summary: It is believed that the organs of severely malnourished children malfunction because harmful compounds called oxidants injure the tissues in these organs. In a healthy person oxidants are made harmless because another compound called glutathione neutralizes them. Glutathione is made from three amino acids that we get from the protein we eat in our food. We found that malnourished children were not making enough glutathione because they lacked one of these amino acids called cysteine. The body is supplied with cysteine made from another amino acid called methionine, from our diet and when our body proteins are broken down. In this study we wanted to find out if children with a form of malnutrition called kwashiorkor were not making enough cysteine because they had a shortage of methionine and also what was causing this shortage . We found that these children produced less methionine because they were breaking down their body proteins at a much slower rate than when they were not malnourished. This finding suggests that dietary supplements of methionine may help malnourished patients produce enough cysteine to make adequate amounts of cysteine thereby protecting their organs from damage by oxidants.

Technical Abstract: Children with edematous but not nonedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentrations of cysteine and methionine, which suggests a decreased availability of methionine for cysteine synthesis. We propose that methionine production and metabolism will be slower in children with edematous SCU than in those with nonedematous SCU. We aimed to measure methionine flux, its transmethylation and its transsulfuration, and homocysteine remethylation in children with SCU. Methionine kinetics were measured in 2 groups of children with edematous (n = 11) and nonedematous (n = 11) SCU 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 had recovered (clinical phase 3). At clinical phase 1, children with edematous SCU had rates of total methionine flux, flux from protein breakdown, and flux to protein synthesis that were slower than the rates of the nonedematous group. There were no significant differences in homocysteine remethylation or methionine transsulfuration and transmethylation between the groups at clinical phase 1. These findings suggest that, in the acutely malnourished and infected state, children with edematous SCU have slower methionine production than do children with nonedematous SCU because of a slower rate of release from protein breakdown. This slower methionine production is not, however, associated with slower rates of methionine transsulfuration and transmethylation or homocysteine remethylation.