Inhibition by Corticosteroids of Glucose Incorporation into Fetuses of Several Strains of Mouse

Wong, Ming D.; Burton, A.F.

doi:10.1159/000240356

Cited by 5 publications

(1 citation statement)

References 7 publications

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“…Determination of l4C-glucose uptake was made as described previously (1). Mice were injected with steroid 60 min prior to the labeled glucose, and the fetuses were removed 15 min later.…”

Section: Methodsmentioning

confidence: 99%

Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Wong¹,

Thomson²,

Burton³

1976

Neonatology

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¹⁴C-glucose uptake by mouse fetuses was reduced by doses of dexamethasone, 200 μg or more, which over 2 days caused fetal death. Uptake by strain C57B1/6J > A/J > SWV. Corticosterone or cortisol, 4 mg, caused neither reduced uptake nor fetal death. These differences occurred despite similar maternal hyperglycemia in all cases. Recovery of ³H-steroid after 15 min, total and unchanged steroid per gram fetal tissue was: corticosterone 1.7 and 0.3 %; dexamethasone 0.12 and 0.06 % of the dose. Rapid metabolism of corticosterone apparently prevents accumulation in fetal tissue sufficient to evoke a response under these conditions.

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“…Determination of l4C-glucose uptake was made as described previously (1). Mice were injected with steroid 60 min prior to the labeled glucose, and the fetuses were removed 15 min later.…”

Section: Methodsmentioning

confidence: 99%

Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Wong¹,

Thomson²,

Burton³

1976

Neonatology

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Cortisone cure of the lidgap defect in fetal mice: A dose‐response and time‐response study

1984

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Cortisone administered during pregnancy prevents the phenotypic expression of lidgap-Miller (lgM1), a genetically determined congenital defect in mice. The dose-response, on a probit log dose scale, is linear to a dose of 60 mg/kg maternal body weight, giving an observed maximum cure of 94% and an ED50(1) of 27 mg/kg. At higher doses the rate of prevention diminishes, to 56% at 320 mg/kg. Fetal (18-day) weight remains unaffected for doses of up to 60 mg/kg and then drops sharply at higher doses, suggesting that cortisone is toxic in this higher range. The severity of lidgap, measured in two ways (as one or both eyes open and as width of gap), decreases as its frequency falls. This finding is in keeping with the threshold model for birth defects. The threshold appears to be in the embryos rather than in their mothers. There is a broad optimum time of treatment: days 13-14 for the 80 mg/kg dose, and days 14-15 for the 30 mg/kg dose. Treatment on day 16 has little or no effect. It is not known how cortisone cures the lidgap trait. The action may be specific--to stimulate transcription of a specific gene, possibly of the lidgap locus itself--or more general, e.g., to alter cell division rate or extracellular matrix constituents.

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Isolation and preliminary characterization of corticosterone-receptor complexes in mouse placental tissue

Wong

Burton

1973

Biochemical and Biophysical Research Communications

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Inhibition by Corticosteroids of Glucose Incorporation into Fetuses of Several Strains of Mouse

Cited by 5 publications

References 7 publications

Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Cortisone cure of the lidgap defect in fetal mice: A dose‐response and time‐response study

Isolation and preliminary characterization of corticosterone-receptor complexes in mouse placental tissue

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