Developmental Changes of Cerebral Ketone Body Utilization in Human Infants

Kraus, H; Schlenker, Stephan; Schwedesky, Dagmar

doi:10.1515/bchm2.1974.355.1.164

Cited by 160 publications

(53 citation statements)

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“…In control subjects and children with grade I PCM, the OGI wa 65.8%. These values are significantly less than those reported for adults (91.9% (7); 88.9% (18)), but are similar to those obtained by Kraus et al (20) on normal German infants (77.4%). With increasing severity of PCM, there was a fall in the OGI, so that in children with grade IV PCM, the OGI was only 34.7%.…”

Section: Resultssupporting

confidence: 84%

Energy Metabolism of Brain in Human Protein-Calorie Malnutrition

et al. 1977

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SummaryCerebral 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 mVlOO glmin, 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 pMI100 glmin, 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 * 5.4 mUl00 glmin, and the OGI was 34.7%. Cerebral lactic add production was 27.4 pM/100 glmin, and the R.Q. rose to 1.52. These findings suggest that in severe human PCM the proportion of glucose ~d e r g o i n g 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. SpeculationThese 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 w i t h 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.Protein-calorie malnutrition is characterized by a variety of neurologic and behavioral symptoms (14, 15). Apathy, withdrawal, and lack of interest in surroundings are the most constant and earliest neurologic features of the condition, and are common in children whose weight is less than 40% of the expected value (29). The electroencephalogram is usually diffusely slowed during the acute stages, returning to normal after nutritional recovery (1 3).Long term studies on children who have experienced PCM early in life demonstrate a variety cf cognitive inadequacies. These result in defective intersensory organization and poor school performance (5,6,8,22,26). As a rule, the younger the child at the time of his hospitalization for malnutrition, the less likely is he to achieve ultimate intellectual parity (4).Numerous experimental studies have been designed to reproduce the clinical picture of PCM. The brain of an animal subjected. to nutritional deprivation in the course of development weighs less, contains fewer cells, and has lesser amounts of protein, nucleic acid, and myelin than the brain of a well nourished animal (l0,21,31-34). From these studies, it has become evident that when nutritional deprivation occurs at the time of the brain's "growth spurt" these alterations are maximal and irreversible (1 0).In order to correlate the data gathered from experimental animals with clinical experience, we undertook...

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Section: Resultssupporting

confidence: 84%

Energy Metabolism of Brain in Human Protein-Calorie Malnutrition

et al. 1977

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“…The av erage CBF in infants was 69 ml 100 g-I min-I. Arte rial concentrations of glucose, lactate, acetoacetate, and 3-hydroxybutyrate were very similar to those reported for infants by Kraus et al (1974) and the arteriovenous difference values for each substrate were also similar in the two studies. Rates of cere bral exchange could be calculated using the CBF measurements, and some of the data are shown in Table 2.…”

Section: Humanssupporting

confidence: 78%

Substrate Utilization and Brain Development

Cremer

1982

J Cereb Blood Flow Metab

167

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“…The utilization of exogeneous galactose in the brain of fetal and newborn mice is still uncertain. Such low radioactivity in the brain of fetal and newborn mice may be related to the fact that the ketone body is the major metabolic fuel in the suckling period (11,17,23,28,29,37). As stated above, radioactivity in the brain increased from 3 weeks after the birth.…”

Section: R-mentioning

confidence: 85%

Whole-body autoradiographic study on the distribution of (U-14C)galactose in adult, pregnant, newborn and infant mice.

Shimono

1984

Acta Histochem. Cytochem

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Developmental Changes of Cerebral Ketone Body Utilization in Human Infants

Cited by 160 publications

References 0 publications

Energy Metabolism of Brain in Human Protein-Calorie Malnutrition

Energy Metabolism of Brain in Human Protein-Calorie Malnutrition

Substrate Utilization and Brain Development

Whole-body autoradiographic study on the distribution of (U-14C)galactose in adult, pregnant, newborn and infant mice.

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