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    Home > Active Ingredient News > Endocrine System > Diabetes Metab Syndr Obes: Study reveals protective effects and mechanisms of alcohol on diabetic osteoporosis.

    Diabetes Metab Syndr Obes: Study reveals protective effects and mechanisms of alcohol on diabetic osteoporosis.

    • Last Update: 2020-10-13
    • Source: Internet
    • Author: User
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    The protective effect of alcohol on diabetic osteoporosis (DOP) and its mechanism remains unclear.
    study, published online in Diabes Metab Syndr Obes, explores whether alcohol enhances the proliferation and differentiation of high blood sugar-induced MC3T3 cells by inhibiting the expression of KDM7A.
    using high glucose (HG) to induce MC3T3 cells and treat them with different concentrations of alcohol.
    the proliferation and mineralization capabilities of MC3T3-E1 cells were determined using CCK-8 and Alizarin red staining, respectively.
    Western blot analyzed the expression of differentiation-related osteoproteins, KDM7A, and proteins associated with the Wnt/β/catenin signaling path.
    use the ALP test kit to detect alkaline phosphatase (ALP) activity.
    results showed that the high glucose-induced MC3T3-E1 cell proliferation capacity and mineralization capacity decreased, ALP activity decreased, were reversed after treatment with alcohol.
    high glucose induction inhibits the expression of KDM7A, Total-β-catenin, Nuclear-β-catenin, and p-GSK3 beta, which can be reversed after treatment with alcohol.
    KDM7A interference increased the expression of Total-β-catenin, Nuclear-β-catenin, and p-GSK3 beta, while KDM7A over-expression was lowered.
    addition, when treated with KDM7A interference, its proliferation and mineralization capacity and ALP activity were improved, while with KDM7A over-expression treatment, its proliferation and mineralization capacity decreased.
    SKL2001 can improve the proliferation, mineralization and ALP activity of MC3T3-E1 cells.
    above, the results show that alcohol regulates the Wnt/β-catenin signaling path through KDM7A, promoting the proliferation and differentiation of bone cells induced by high blood sugar.
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