AKR1D1 Regulates Glucocorticoid Availability and Glucocorticoid Receptor Activation in Human Hepatoma Cells

    Νικόλαος Νικολάου, Laura Gathercole, Lucy Kirkwood, J E Dunford, Beverly Hughes, Lorna Gilligan, U. Oppermann, T.M. Penning, Wiebke Arlt, Leanne Hodson, Jeremy Tomlinson
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    Finasteride →

    Frontline, gold standard treatment for combatting androgenic alopecia

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    Heavy duty finasteride that comes with higher risks

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    Studysummary This study found that manipulating AKR1D1 expression in human liver cells effectively regulates glucocorticoid clearance and receptor activation, highlighting its role in liver-specific steroid hormone regulation.
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    The study demonstrated that AKR1D1, a steroid A-ring reductase predominantly expressed in the liver, played a significant role in regulating glucocorticoid availability and receptor activation in human hepatoma cells. Over-expression of AKR1D1 increased glucocorticoid clearance and decreased glucocorticoid receptor activation and target gene expression, while knockdown of AKR1D1 had the opposite effect. Additionally, 5α-reductase inhibitors finasteride and dutasteride did not inhibit AKR1D1 activity. These findings suggested that AKR1D1 could be crucial in regulating both endogenous and exogenous glucocorticoid actions, impacting liver-related physiological and pathophysiological processes.
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