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Glucocorticoid regulation of amino acid transport in primary human trophoblast cells

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The effects of glucocorticoids on macronutrient transport in the placenta are not well understood. The dose and length of maternal glucocorticoid use can have varying effects on fetal nutrient acquisition and placental anabolic signaling. In this paper, Vaughan et al. demonstrate that glucocorticoids promote placental anabolic signaling and System A amino acid transport in the presence of insulin in primary human trophoblasts.

To determine the effects of glucocorticoids on placental mechanistic target of rapamycin complex (mTORC) signaling and amino acid uptake, syncytialised primary human trophoblasts were cultured with cortisol or dexamethasone in the presence or absence of insulin. The authors observed insulin responsiveness in these cells with Akt and mTORC1 signaling regardless of glucocorticoid treatment. In fact, they found modest elevations of both signaling pathways after glucocorticoid treatment in the presence of insulin. This was concordant with elevated System A but not System L transporter activity. Despite increasing System A uptake, dexamethasone and cortisol caused reductions in gene expression of System A transporters with and without insulin and did not alter protein abundance, potentially suggesting post-translational mechanisms by which insulin and glucocorticoids promote amino acid transport. These findings highlight the short-term anabolic effects of glucocorticoids on placental amino acid transport and suggest that, similar to the brain, glucocorticoids may promote nutrient flux to those critical tissues during times of stress.

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