Cellular Response with Increased Feeding in Neonatal Rats

Winick, Myron; Noble, Adele

doi:10.1093/jn/91.2.179

Cited by 106 publications

(23 citation statements)

References 5 publications

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“…The study of overnutrition and obesity in female adolescents [25] revealed, as in experimental animals [11,76,133,135], that an increase in the number of nuclei and overgrowth of lean tissues occurs. Obese girls with advanced bone age all had increases in mus<le mass and DNA content within the muscle mass when body length was used as the base line.…”

mentioning

confidence: 99%

Skeletal Muscle Cell Mass and Growth: The Concept of the Deoxyribonucleic Acid Unit

et al. 1971

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mentioning

confidence: 99%

Skeletal Muscle Cell Mass and Growth: The Concept of the Deoxyribonucleic Acid Unit

et al. 1971

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“…Overnutrition in infancy which has been shown to produce overgrowth [18] may play an extremely important role in determining changes in number and size of cells in different tissues [20,43]. Such changes may be irreversible if they persist into adolescence or early life [G, 25].…”

Section: Discussionmentioning

confidence: 99%

Correlative Studies in Obese Children and Adolescents Concerning Body Composition and Plasma Insulin and Growth Hormone Levels

et al. 1971

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“…During the first 3 weeks the weight of the rat cerebrum increases about 8-fold and that of the cerebellum 20-fold (57). Between the ages 5 and 17 days, DNA increases 2.5 times in the cerebrum but 8.5 times in the cerebellum (58). New cell formation is vigorous during the first 21 days after birth, and new cell formation accounts for 59%o of the final number of cells in the cerebrum and 97%o of the final number of cells in the cerebellum (59).…”

Section: Environmental Health Perspectivesmentioning

confidence: 99%

Animal Models of Human Disease: Severe and Mild Lead Encephalopathy in the Neonatal Rat

Michaelson¹,

Sauerhoff²

1974

Environ Health Perspect

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Inorganic lead produces cerebral dysfunction and clinically definable encephalopathies in man. To date there have been few studies on the biochemical changes in brain following exposure to inorganic lead. Studies correlating toxicity with behavioral and brain neurochemical changes following lead exposure have been hindered because adult laboratory animals are resistant to the central nervous system effects of lead poisoning. Such studies have been impeded by lack of suitable experimental models until Pentschew and Garro showed that brain lesions develop In neonatal rats when a pregnant rat newly delivered of her litter is placed on a 4% lead carbonate containing diet. Lead passes into the developing sucklings via maternal milk. Lead-poisoned newborns have pronounced retardation of growth and during the fourth week of ilfe develop the severe signs of lead encephalopathy, namely, extensive histological lesions of the cerebellum, brain edema, and paraplegia. There is an approximate 85-fold increase in the lead concentration of both the cerebellum and cerebral cortex relative to controls, but edema and gross vascular changes are confined to the cerebellum. Ingested lead had little effect on RNA, DNA, and protein concentrations of developing rat cerebellum and cerebral cortex. However, there was a reduction of between 10 and 20% in the DNA content of the cerebellum around 3 weeks of age in the lead-exposed sucklings. This suggests a failure of cell multiplication in this part of the brain.A critical evaluation of this experimental approach indicated that under similar dietary conditions experimental lactating rats eat 30% less food than controls resulting in: (a) sustained loss in body weight of nursing mothers and that (b) offsprings who develop paraplegia and cerebellar damage do so after gaining access to lead containing diet.We have studied mothers' food consumption and body weight changes and blood, milk, and brain lead content; and newborns' body and brain weight changes, blood and brain lead content, and brain serotonin (5HT), norepinephrine (NE), dopamine (DA), and -y-aminobutyric acid (GABA). We have found that a lactating mother rat eating 5% lead acetate (2.73% Pb) produced milk containing 25 ppm lead. When the mothers' diet is changed at day 16 from 5% PbAc to one containing 25 ppm Pb, and neonates allowed free access to the solid diet, the sucklings still have retarded body growth but do not develop paraplegia or grossly apparent vascular damage of the cerebellum. However, during the fourth week these animals exhibit a less severe form of "encephalopathy" consisting of hyperactivity, tremors, and stereotype behavior. Pair-fed controls coetaneous to experimental groups do not display such activities. There was no change in brain 5HT, GABA, or NE, but a 15-20% decrease in brain DA. Change in DA relative to other monoamines suggests a relationship between CNS dysfunction due to lead and DA metabolism in the brain.The experimental design as discribed provides a model of CNS dysfunction due to lead exposure w...

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Cellular Response with Increased Feeding in Neonatal Rats

Cited by 106 publications

References 5 publications

Skeletal Muscle Cell Mass and Growth: The Concept of the Deoxyribonucleic Acid Unit

Skeletal Muscle Cell Mass and Growth: The Concept of the Deoxyribonucleic Acid Unit

Correlative Studies in Obese Children and Adolescents Concerning Body Composition and Plasma Insulin and Growth Hormone Levels

Animal Models of Human Disease: Severe and Mild Lead Encephalopathy in the Neonatal Rat

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