Energy Metabolism of Brain in Human Protein-Calorie Malnutrition

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Abstract
Summary: 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 μM/100 g/min, and the respiratory quotient (R.Q.) was 1.00. With increasing severity or PCM, there was increased glucose utilization and a progressive reduction in the OGI. In grade IV PCM, CBF was 68.7 ± 5.4 ml/100 g/min, and the OGI was 34.7%. Cerebral lactic add production was 27.4 pM/100 g/min, and the R.Q. rose to 1.52. These findings suggest that hi severe human PCM the proportion of glucose undergoing aerobic oxidation is reduced, and that in addition to being converted to tactic acid, a significant proportion of glucose is transformed by the brain into long chain fatty acids. Speculation: These results indicate that in chronic, severe PCM, a considerable proportion of glucose utilized by the brain is converted into fatty acids. This alteration in cerebral carbohydrate metabolism may be due to altered function of one or more of the regulatory enzymes within the brain. Acetyl coenzyme A carboxylase, fatty add synthetase, and the hexose monophosphate shunt dehydrogenases are some of the more obvious candidates for future investigations.