The Growth Retarded Fetus

Warshaw, Joseph B.

doi:10.1016/s0095-5108(18)31153-9

Cited by 5 publications

(2 citation statements)

References 38 publications

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“…In the intra-uterine growth-retarded human neonate hypoglycaemia is a common phenomenon and if uncorrected can lead to cerebral damage or death (Warshaw, 1979). Our studies in the piglet indicate that although both the rate of glucose utilization and the total body-glucose pool size are reduced in intrauterine growth-retarded animals they are appropriate for their reduced body weight.…”

Section: Discussionmentioning

confidence: 63%

Total Body-Glucose Turnover in Normal and Intra-Uterine Growth-Retarded Neonatal Piglets

1981

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1. Because studies of the metabolic problems of the human intra-uterine growth-retarded neonate are limited by ethical considerations we have used the intra-uterine growth-retarded piglet as an animal model. Total body-glucose kinetics were measured in 16 intra-uterine growth-retarded and 11 normal piglets from the same litters with [3H]glucose as a tracer. 2. The intra-uterine growth-retarded animals had marginally smaller brains than their normal littermates, but substantially smaller livers. Liver weight was reduced in proportion to body weight. 3. Total body-glucose turnover rate was significantly lower (P less than 0.001) in the intra-uterine growth-retarded animals in comparison with their normal littermates, but was appropriate for their smaller body and liver weights. Brain weight was only slightly reduced in the intra-uterine growth-retarded group so that glucose turnover adjusted to a common brain weight was significantly lower (P less than 0.001) in these animals. 4. Total body-glucose pool size was lower in the intra-uterine growth-retarded animals (P less than 0.01), but was appropriate for their body and liver weights. It was significantly reduced in relation to brain weight (P less than 0.001). 5. Resting plasma glucose concentration was lower in the intra-uterine growth-retarded animals (P less than 0.001). There was no relationship between concentration and turnover in either group. 6. It is suggested that the observed differences in total body-glucose turnover may be associated with profound differences in cerebral metabolism in the intra-uterine growth-retarded animals.

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Section: Discussionmentioning

confidence: 63%

Total Body-Glucose Turnover in Normal and Intra-Uterine Growth-Retarded Neonatal Piglets

1981

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“…A redistribution of blood flow within the fetus during intrauterine starvation and hypoxia may supply nutrients and oxygen to brain tis sue at the expense of other fetal organs [2,23]. When maternal starvation was suffi ciently severe (3 g pellet/24 h) it proved le thal.…”

Section: Discussionmentioning

confidence: 99%

Somatic Growth and Brain Development

Meberg¹

1981

Neonatology

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Groups of female mice were starved or exposed to hypobaric hypoxia during pregnancy. A significantly lower weight gain during pregnancy occurred in the mothers starved or exposed to hypoxia compared to controls. Hypoxia also decreased maternal food intake. Therefore, the hypoxic groups included a combination of hypoxia and starvation. Body weight, brain weight, brain DNA (deoxyribonucleic acid) and total protein were investigated in the offspring at birth and at 20 and 70 days of age. Starvation and hypoxia impaired fetal growth, with reduction in body weight, brain weight, brain cell number (DNA content) and brain total protein content in a dose-related manner. In the most severely starved fetuses brain cell size (brain weight/DNA and total protein/DNA) was also reduced. Long-term effects were observed with lower body weight, brain weight and brain DNA content at adult age in the most severely malnourished and hypoxic offspring. Catch-up growth took place after a more moderate starvation and hypoxic exposure. It is concluded that intrauterine malnutrition interferes with fetal cellular mitotic rate. This may give rise to growth-retarded fetuses because of a decreased cell number. Depending on the degree of malnutrition a cell deficit may persist at adult age. Intrauterine hypoxia may aggravate these effects of fetal starvation.

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Abel

1984

Fetal Alcohol Syndrome and Fetal Alcohol Effects

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The Growth Retarded Fetus

Cited by 5 publications

References 38 publications

Total Body-Glucose Turnover in Normal and Intra-Uterine Growth-Retarded Neonatal Piglets

Total Body-Glucose Turnover in Normal and Intra-Uterine Growth-Retarded Neonatal Piglets

Somatic Growth and Brain Development

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