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
    Image of study
    TLDR AKR1D1 controls glucocorticoid levels and receptor activity in liver cells.
    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.
    Discuss this study in the Community →

    Cited in this study

    2 / 2 results