Cell Composition and Metabolism in Kwashiorkor (Severe Protein-Calorie Malnutrition in Children)

Metcoff, Jack; Frenk, Silvestre; Yoshida, Takashi; Pinedo, Ramon Torres; Kaiser, Elizabeth; Hansen, Jo‐Ida C.

doi:10.1097/00005792-196609000-00002

Cited by 50 publications

(27 citation statements)

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“…It therefore seems reasonable to infer that these diminished enzyme activities were related to the reduced nutritional intake of this infant during the last month of his life rather than to his ketoacidosis. The terminal malnutrition of this infant might also explain the increased inhibitory effect of phenylalanine on the muscle pyruvate kinase of this infant since similar effects by both competitive and noncompetitive inhibitors on this enzyme have been observed by Metcoff (26). In contrast, it has been demonstrated that extended starvation does not affect CoA-transferase in rats (8,9).…”

Section: Methodsmentioning

confidence: 51%

“…2 A similar conclusion might also be appropriate for the reduced activities obtained for glycolytic enzymes. However, it has been reported that prolonged malnutrition causes a reduction in the specific activities of several glycolytic enzymes (26). It therefore seems reasonable to infer that these diminished enzyme activities were related to the reduced nutritional intake of this infant during the last month of his life rather than to his ketoacidosis.…”

Section: Methodsmentioning

confidence: 82%

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Succinyl-CoA: 3-Ketoacid CoA-Transferase Deficiency. A CAUSE FOR KETOACIDOSIS IN INFANCY

Tildón¹,

Cornblath²

1972

J. Clin. Invest.

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Section: Methodsmentioning

confidence: 51%

Section: Methodsmentioning

confidence: 82%

Succinyl-CoA: 3-Ketoacid CoA-Transferase Deficiency. A CAUSE FOR KETOACIDOSIS IN INFANCY

Tildón¹,

Cornblath²

1972

J. Clin. Invest.

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“…Alternatively, changes in the proportion of Na+ and K+ could result from a deficit in brain carbohydrate metabolism as has been proposed for muscle tissue of malnourished children [3,15,16]. This seems to be unlikely in the case of brain since glycolytic rate in •vitro (lactate production from glucose) was not affected by growth retardation.…”

Section: Discussionmentioning

confidence: 98%

Effects of Growth Retardation and Asphyxia on Brain Electrolytes and on Glycolysis in Developing Rats

1973

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ExtractDuring postnatal brain development in the rat there is a progressive decrease in the Na + /K + ratio, which correlated with increasing activity of Na + -K+-activated ATPase. Undernutrition during intrauterine and early postnatal development (4-6 days) did not alter the Na + /K+ ratio, although there was a deficit in brain weight. However, undernutrition during the suckling period retarded the progressive fall in Na+/K+ ratio and rise in ATPase activity. The altered Na+/K + ratio in these animals did not appear to be caused by change in brain carbohydrate metabolism.Developing rats undernourished until 4-6 days resembled the intrauterine growthretarded human baby as regards deficits in body weight, relative sparing of the brain compared with other organs, and depleted carbohydrate reserves.The undernourished 4-6-day-old rat tolerated asphyxia as well as the well nourished rat of the same age. After asphyxia, the Na+/K+ ratio reverted to unity and there was an increase in brain water. Liver carbohydrate reserves did not appear to be a limiting factor that determined the point of death. Speculation

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“…water with increased concentrations of sodium (Na) and inorganic phosphate (Pi) in the muscle cell, while concentrations of potassium (K) and magnesium (Mg) are reduced [1][2][3]. Very similar results were reported by Broyer et al and Bergstrom's group in uremie patients [4][5][6].…”

Section: Cellular Malnutrition In Pcmmentioning

confidence: 71%

“…In children with severe protein-calorie malnutrition (PCM), true Kwashiorkor, cellular abnormalities in electrolytes, enzymes, and metabolites in the energy-generating pathways were identified many years ago [1][2][3]. More recently, similar defects have been found in muscle [4][5][6] and/or leukocytes [7][8][9] of patients with chronic renal failure, along with abnormal intracellular (i.e.)…”

Section: Introductionmentioning

confidence: 99%

Malnutrition at the cellular level in uremia: a new frontier for research.

Metcoff¹

1986

Journal of the American College of Nutrition

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Previously reported studies showed that protein-calorie malnutrition (PCM) in children is associated with significant alterations in muscle cell composition, characterized by increased cell water and Na, with decreased concentrations of K, Mg, and some glycolytic and citric acid cycle metabolites. In PCM, the i.c. H2O and levels of Na and K were significantly related, by multiple regression analysis, to the combined set of simultaneously measured levels of cell metabolites, phosphoenolpyruvate, pyruvate, alpha-ketoglutarate, and oxaloacetate. Cell bioactivities also were affected by PCM. Activities of the enzymes pyruvate kinase and malic and isocitric dehydrogenases were significantly reduced in muscle homogenates of PCM children. Kinetic analysis of pyruvate kinase indicated an 8-10-fold reduction in maximal velocity of the enzyme, consistent with a reduction in enzyme protein. Additionally, reduced levels of ATP and the equilibrium constant of the adenylate kinase system were observed in leukocytes of PCM children. Alterations in the activity of the energy-dependent Na pump have been noted by others in association with the accumulation of i.c. Na in severe malnutrition. Neither protein synthesis nor amino acid pools was measured in these previously reported studies. Recent data from several laboratories show that the "profiles" of i.c. and plasma amino acids are very different, both in uremics and in control subjects. In control subjects, with leukocytes as the cell model, the level of protein synthesis can be predicted by multiple regression analyses from simultaneously measured levels of plasma or i.c. amino acids. Intracellular amino acids are better predictors. Of 19 intracellular amino acids, a combination of five accounted for 54% of the variance in protein synthesis in normal, healthy adults. Levels of these predictor cell amino acids can, in turn, be predicted by different combinations of apparently unrelated plasma amino acids. In adult uremic patients stabilized by hemodialysis, with leukocytes as the cell model, levels of ATP, energy charge, adenylate kinase and pyruvic kinase activities were reduced. Others have reported increased i.c. water and Na contents, and impaired Na pump activity. Cell levels of methionine and the branched-chain amino acids, valine, leucine, and isoleucine, and protein synthesis also were significantly reduced. By multiple regression analysis, the observed levels of protein synthesis and energy charge in the hemodialyzed uremic patients were largely accounted for by different combinations of intracellular amino acid than in healthy subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

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Cell Composition and Metabolism in Kwashiorkor (Severe Protein-Calorie Malnutrition in Children)

Cited by 50 publications

References 0 publications

Succinyl-CoA: 3-Ketoacid CoA-Transferase Deficiency. A CAUSE FOR KETOACIDOSIS IN INFANCY

Succinyl-CoA: 3-Ketoacid CoA-Transferase Deficiency. A CAUSE FOR KETOACIDOSIS IN INFANCY

Effects of Growth Retardation and Asphyxia on Brain Electrolytes and on Glycolysis in Developing Rats

Malnutrition at the cellular level in uremia: a new frontier for research.

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