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Energy metabolism of brain in human protein-calorie malnutrition
Insights
Protein-calorie malnutrition (PCM) in children impairs brain glucose metabolism. Severe PCM reduces aerobic glucose oxidation, converting more glucose to lactic acid and fatty acids.
Area of Science:
- Pediatric Nutrition
- Neuroscience
- Metabolic Disorders
Background:
- Protein-calorie malnutrition (PCM) is a significant health concern in children.
- Understanding its impact on brain function is crucial for effective intervention.
Purpose of the Study:
- To investigate cerebral blood flow (CBF) and carbohydrate metabolism in children with varying degrees of PCM.
- To elucidate the alterations in brain glucose utilization and energy production.
Main Methods:
- Studied CBF and oxygen/glucose index (OGI) in normal children and those with PCM (aged ≤40 months).
- Measured cerebral lactic acid production and respiratory quotient (R.Q.).
Main Results:
- Normal CBF and OGI (65.8%) in healthy children and mild PCM, with significant lactic acid production.
- Increased glucose utilization and reduced OGI (34.7%) in severe PCM (Grade IV).
- Elevated R.Q. (1.52) in severe PCM, indicating reduced aerobic glucose oxidation.
Conclusions:
- Severe PCM alters brain carbohydrate metabolism, reducing aerobic glucose oxidation.
- The brain converts glucose to lactic acid and long-chain fatty acids in severe PCM.
- These metabolic shifts highlight the profound neurological impact of malnutrition.
Abstract:
Cerebral blood flow (CBF) and carbohydrate metabolism were studied in 5 normal children and 25 children, aged 40 months or less, with varying degrees of protein-calorie malnutrition (PCM). CBF in normal children and those suffering from grade I PCM was 90.3 +/- 5.7 ml/100 g/min, a value comparable with that obtained by other investigators, but the proportion of glucose taken up by the brain which combined with oxygen, the oxygen/glucose index (OGI), was 65.8%, indicating significant conversion of glucose into lactic acid. Cerebral lactic acid production was 45.3 micronM/100 g/min, and the respiratory quotient (R.Q.) was 1.00. With increasing severity of PCM, there was increased glucose utilization and a progressive reduction in the OGI. In grade IV PCM, CBF was 68.7 +/- 5.4ml/100g/min, and the OGI was 34.7%. Cerebral lactic acid production was 27.4 micronM/100 g/min, and the R.Q. rose to 1.52. These findings suggest that in severe human PCM the proportion of glucose undergoing aerobic oxidation is reduced, and that in addition to being converted to lactic acid, a significant proportion of glucose is transformed by the brain into long chain fatty acids.