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  • Iron In Osteoporosis

    From ironjustice@21:1/5 to All on Mon Feb 26 07:11:22 2018
    Osteoporosis in chronic liver disease
    Reviews
    Authors
    Núria Guañabens, Albert Parés
    Accepted manuscript online: 26 February 2018
    DOI: 10.1111/liv.13730
    Abstract
    Osteoporosis is a frequent complication in patients with chronic liver disease, especially in end-stages and in chronic cholestasis, in addition to nonalcoholic fatty liver disease, hemochromatosis and alcoholism. Mechanisms underlying osteoporosis are
    poorly understood, but osteoporosis mainly results from low bone formation. In this setting, sclerostin, a key regulator of the Wnt/ß-catenin signalling pathway which regulates bone formation, in addition to the effects of the retained substances of
    cholestasis such as bilirubin and bile acids on osteoblastic cells, may influence the decreased bone formation in chronic cholestasis. Similarly, the damaging effects of iron and alcohol on osteoblastic cells may partially explain bone disease in
    hemochromatosis and alcoholism. A role for proinflamatory cytokines has been proposed in different conditions. Increased bone resorption may occur in cholestatic women with advanced disease. Low vitamin D, poor nutrition and hypogonadism, may be
    contributing factors to the full picture of bone disorders in chronic liver disease.

    This article is protected by copyright. All rights reserved.

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  • From ironjustice@21:1/5 to All on Wed Apr 18 08:13:05 2018
    Hepcidin is an endogenous protective factor for osteoporosis by reducing iron levels
    Peng Zhang1,*, Sheng Wang2,*, Liang Wang3,*, Bin Chen Shan1,*, Hui Zhang4, Fan Yang4, Zhi Qiang Zhou1, Xiao Wang4, Ye Yuan4 and You Jia Xu1,4⇑
    1Department of Orthopaedics,
    the Second Affiliated Hospital of Soochow University, Suzhou, China
    2Emergency Department,
    Zhongshan Hospital Affiliated to Fudan University, Shanghai, China
    3Department of Radiology,
    Children's Hospital of Soochow University, Suzhou, Jiangsu, China
    4Osteoprosis Institute of Soochow University,
    Suzhou, China
    Correspondence should be addressed to Y J Xu: xuyoujia at suda.edu.cnsuda

    Abstract
    Postmenopausal osteoporosis is a global health issue. Although a lack of estrogen is considered the major reason for postmenopausal osteoporosis, other factors might also contribute the etiology of the disease. In previous reports, we and others proposed
    that iron accumulation after menopause accelerates osteoporosis, and here, we genetically modified the expression of an endogenous hormone, hepcidin, to modulate iron status in a mouse model. Our results show that hepcidin levels negatively correlate
    with bone loss in both knockout and overexpression (with ovariectomy) murine models. In addition, iron overload enhances reactive oxygen species (ROS) activity and attenuates the functions of primary osteoblasts, while iron depletion could reverse this
    phenomenon through inhibiting the functions of primary osteoclasts. Therefore, our results provide more evidence of the ‘iron accumulation’ hypothesis, which suggests that high iron levels are risk factors for osteoporosis, and the ‘Huang’s
    hypothesis’ that hepcidin is a potential drug target for the prevention of postmenopausal osteoporosis.

    Keywords
    hepcidin osteoporosis oxidative stress bone metabolism iron metabolism
    Received 19 February 2018
    Accepted 21 March 2018
    Made available online as an Accepted Preprint 21 March 2018
    © 2018 Society for Endocrinology

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