Low Content of Cerebral Lipids in Infants suffering from Malnutrition

Fishman, Marvin A.; Prensky, Arthur L.; Dodge, Philip R.

doi:10.1038/221552a0

Cited by 64 publications

(25 citation statements)

References 22 publications

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“…Fetal malnutrition has been associated with decreased myelin content in the brain (5,6,12). In this study, this effect has not been observed in diabetic animals.…”

Section: Discussionsupporting

confidence: 50%

“…It is well known that diabetes may affect fetal growth and predisposes to prematurity. Therefore, it is essential to consider these two variables together, especially since maturity and nutritional status affect fetal brain development (3,6,12,29,30). Accordingly, positive correlations were found in this study between cerebrum weights and fetal weights over a wide range of fetal weight values.…”

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

“…Consequently, diabetic pregnancy has been proposed as a new model of fetal malnutrition (23). While it has been shown that those parameters such as brain weight, cell number, protein content, and myelination were affected in situations of fetal malnutrition (3,6,12,29,30) these characteristics of fetal brain development have not been investigated in diabetic pregnancies.The goal of this study was to investigate fetal brain development during diabetic pregnancies, with regard to cerebral and cerebellar DNA, protein content, and myelination (cerebrosidesulfatide content). In order to detect any specific effects of diabetes on brain development, other organs such as the liver and placenta were also examined.…”

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confidence: 99%

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Fetal Brain Development in Diabetic Guinea Pigs

Saintonge

Côté

1984

Pediatr Res

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SummaryFetal brain development was investigated near term in guinea pigs rendered diabetic with streptozotocin. The liver and the placenta were used as reference organs. Compared to controls, those fetuses from diabetic animals had normal cerebrum and cerebellum weights, but higher liver and placenta weights in relation to fetal weights. Although liver and placenta cell number (DNA content) was unchanged, it was significantly increased in the fetal cerebrum and cerebellum of diabetics. Although the tissue protein concentration was decreased in the liver and the placenta, it was unchanged and even increased in the cerebrum and cerebellum, respectively. The concentration of myelin (cerebroside-sulfatide) was unchanged in the cerebrum, but it was increased in the cerebellum of diabetic animals.These data suggest that diabetes has a growth-promoting effect on the fetal brain cell number. Furthermore, differences in the protein content between fetal organs may reflect abnormalities in protein metabolism which do not affect the brain during diabetic pregnancies.Textbooks of pediatrics and neonatology have repeatedly reported low brain weights in relation to body weights in macrosomic babies of diabetic mothers (2, 1 1, 24, 27). Gruenwald (1 4) has reported that the rate of growth of human fetal brain is diminished in diabetic pregnancies past 30 weeks of gestation. Decreased fetal brain weight in diabetic pregnancies has also been reported by Driscoll et ul. (10) suggesting that maternal diabetes may interfere with fetal brain development.In a recent study, a decreased placental transfer of amino acids to the fetus was found in diabetic guinea pigs (22). Consequently, diabetic pregnancy has been proposed as a new model of fetal malnutrition (23). While it has been shown that those parameters such as brain weight, cell number, protein content, and myelination were affected in situations of fetal malnutrition (3,6,12,29,30) these characteristics of fetal brain development have not been investigated in diabetic pregnancies.The goal of this study was to investigate fetal brain development during diabetic pregnancies, with regard to cerebral and cerebellar DNA, protein content, and myelination (cerebrosidesulfatide content). In order to detect any specific effects of diabetes on brain development, other organs such as the liver and placenta were also examined. The guinea pig was selected as the model in view of its brain maturity at birth which approaches the human situation more than other species (1,5,8,9).Female guinea pigs of the Hartley strain were fed a standard diet (guinea pig chow, Ralston Purina), with free access to water, and were maintained under normal laboratory conditions. Because insulin-induced hypoglycemia potentiates the diabetogenic activity of streptozotocin in this species (4,15,20), the animals were given streptozotocin (1 50 mg/kg) IV (diabetic animals) or an equivalent amount of a saline solution (control animals) 90 min after one IV injection of 15 units of crystalline insulin.After mating, day 1...

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“…Fetal malnutrition has been associated with decreased myelin content in the brain (5,6,12). In this study, this effect has not been observed in diabetic animals.…”

Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Fetal Brain Development in Diabetic Guinea Pigs

Saintonge

Côté

1984

Pediatr Res

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“…There is evidence since the 1950's and 1960's that protein-calorie malnutrition is associated with retarded brain growth (Stock & Smythe, 1963), reduced cerebral cellularity (Winick & Rosso, 1969),reduced myelination (Fishman, Prensky, & Dodge, 1969) and, in the neurophysiological field, changes in electroencephalogram (Engel, 1956;Nelson & Dean, 1959) and evoked potential tracings (Kawai, Nakamura, & Matsuo, 1989;Flinn, Barnet, Lydick, & Lackner, 1993;Hernández et al, in press).…”

mentioning

confidence: 99%

Effects of Malnutrition and Sensory-Motor Stimulation on Auditory Evoked Potentials

Lima¹,

Funayama²,

Oliveira³

et al. 2016

REBAC

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There is evidence that the auditory evoked potential (AEP) is altered by malnutrition both in laboratory animals and in humans. The objective of the present study was to determine whether changes in the AEP caused by malnutrition could be reversed by nutritional rehabilitation and sensorymotor and environmental stimulation during hospitalization. Six children aged 5-33 months with severe malnutrition (kwashiorkor, marasmus and marasmic-kwashiorkor) were admitted to the Pediatric Ward of a University Hospital. Normal age and sex-matched children from the hospital day-care center were enrolled as a control group. The AEP was tested in an electrically and acoustically isolated room using a Nicolet CA 2000 microcomputer. Clicks of 90; 80; 70 and 60 dBn HL were presented through earphones. The results suggest that malnutrition leads to an increase in wave I latencies in patients with marasmus, and in waves I, III and V in those with kwashiorkor or marasmic-kwashiorkor type at 90 dB HL. At discharge, all but one patient with kwashiorkor showed reduced latencies of waves I, III and V compared to the values on admission. Despite the small sample, these preliminary results pointed out that the process of sensory stimulation used in our study in a properly directed, systematic and individualized manner showed encouraging results in terms of AEP recovery in these children.

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