Effect of a Transcriptionally Inactive or Absent Vitamin D Receptor on Beta-Cell Function and Glucose Homeostasis in Mice

    November 2016 in “ Journal of steroid biochemistry and molecular biology/˜The œJournal of steroid biochemistry and molecular biology ”
    Pieter Gillard, Heidi Wolden-Kirk, Katleen Lemaire, Annemieke Verstuyf, Lieve Verlinden, Yasutake Yamamoto, Shigeaki Kato, Leentje Van Lommel, Frans Schuit, Bart Van der Schueren, Chantal Mathieu, Lut Overbergh
    TLDR Mice without active or present vitamin D receptors maintain normal blood sugar control and islet gene expression when calcium levels are normal.
    Researchers studied the impact of a transcriptionally inactive or absent vitamin D receptor (VDR) on beta-cell function and glucose homeostasis in mice by comparing VDRΔAF2, VDR knockout (VDR−/−), and wild type (WT) mice. Despite variations in body weight and fat percentage, glucose tolerance and insulin secretion were similar across all groups. Only one gene, phosphodiesterase 10a, was differentially expressed, being upregulated in both VDRΔAF2 and VDR−/− islets. The study concluded that under normocalcemic conditions, the absence of VDR or its ligand-activated transcription did not affect glucose homeostasis or beta-cell function in mice.
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