alexa Chronic ethanol exposure inhibits insulin and IGF-1 stimulated amino acid uptake in cultured human placental trophoblasts.
Diabetes & Endocrinology

Diabetes & Endocrinology

Journal of Steroids & Hormonal Science

Author(s): Karl PI, Fisher SE

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Abstract Maternal alcohol abuse during pregnancy can lead to abnormalities in fetal development, sometimes manifested as the fetal alcohol syndrome (FAS). Although intrauterine growth retardation is a hallmark of FAS, the pathophysiology is not fully understood. A contributing factor may be altered placental function. In this study, the effect of long-term exposure to ethanol on subsequent amino acid uptake by the cultured human placental trophoblasts was examined. Both Na(+)-dependent and Na(+)-independent pathways for AIB uptake were measured. As reported previously, insulin and IGF-1 enhanced Na(+)-dependent AIB uptake. Exposure to ethanol had no effect on basal (nonhormone treated) AIB uptake. However, 72-hr ethanol pretreatment of trophoblasts inhibited Na(+)-dependent AIB uptake under stimulation by insulin or IGF-1 in the absence of ethanol. Na(+)-independent uptake was not affected. Ethanol treatment had no effect on insulin or IGF-1 binding to cultured trophoblasts. These findings suggest that 72-hr ethanol treatment in cultured trophoblasts may affect postreceptor signal transduction in the insulin or IGF-1 pathways. Such changes have implications for the effect of ethanol on normal function of the human placenta, the major interface for maternal/fetal transfer of nutrients.
This article was published in Alcohol Clin Exp Res and referenced in Journal of Steroids & Hormonal Science

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