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Chunyu Wang, Li Tian, Kun Zhang, Yaxi Chen, Xiang Chen, Ying Xie, Qian Zhao and Xijie Yu

reduces bone mineral density (BMD) in mice ( Halade et al . 2010 ). Obesity affects bone metabolism through several potential mechanisms. It is well known that both adipocytes and osteoblasts are derived from the same progenitor cells: bone marrow

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Siyi Zhu, Hongchen He, Chengfei Gao, Guojing Luo, Ying Xie, Haiming Wang, Li Tian, Xiang Chen, Xijie Yu and Chengqi He

Introduction Sex steroids play a regulatory role in bone metabolism. After menopause, declining estrogen levels combined with a parallel increase in follicle-stimulating hormone (FSH) levels disrupt the orchestrated balance between bone

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Peng Zhang, Sheng Wang, Liang Wang, Bing Chen Shan, Hui Zhang, Fan Yang, Zhi Qiang Zhou, Xiao Wang, Ye Yuan and You Jia Xu

, Jiang et al . 2016 ). To further investigate the effects of hepcidin on bone metabolism, we made use of FAC and DFO to simulate hepcidin deficiency and overexpression conditions in cultured osteoblasts and osteoclasts. Our results show that the

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Xin-wei Chen, Ye-hong Li, Meng-jun Zhang, Zhou Chen, Dian-shan Ke, Ying Xue and Jian-ming Hou

physiologically pleiotropic properties, such as antioxidant ( Kruzel et al. 2002 ) anti-inflammatory and anti-tumor effects, as well as the regulation of bone metabolism. Indeed, Bharadwaj et al . found that following an oral supplementation of LF, bone

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Yingyu Feng, Lei Su, Xing Zhong, Wei Guohong, Haipeng Xiao, Yanbing Li and Lingling Xiu

osteoporosis ( Kurra & Siris 2011 ). In addition, patients with both diabetes and osteoporosis are increasingly common in an aging society ( Viegas et al. 2011 ). The effects of antidiabetic agents on bone metabolism have thus received increased attention

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Yasmine Hachemi, Anna E Rapp, Ann-Kristin Picke, Gilbert Weidinger, Anita Ignatius and Jan Tuckermann

detail on bone metabolism in vivo . For the GR modulator AL-438 selected on the base of differential co-regulator recruitment, a clear lower suppression of bone formation rate was described, thus sparing GC effects on bone ( Coghlan et al . 2003

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M Rodríguez-Sanz, N García-Giralt, D Prieto-Alhambra, S Servitja, S Balcells, R Pecorelli, A Díez-Pérez, D Grinberg, I Tusquets and X Nogués

that estrogen and vitamin D endocrine systems play an important role in bone metabolism ( Felson et al . 1993 , Cranney et al . 2007 ). Depletion of any of these hormones leads to a bone mass reduction, which in some cases is very severe ( Eriksen

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Maxime A Tremblay, Raifish E Mendoza-Villarroel, Nicholas M Robert, Francis Bergeron and Jacques J Tremblay

al. 1999 ). During adult life, INSL3 was found to regulate bone metabolism in males ( Ferlin et al. 2008 , 2013 ). In addition to its important functional roles, INSL3 constitutes a highly specific marker of Leydig cell differentiation and

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Raifish E Mendoza-Villarroel, Mickaël Di-Luoffo, Etienne Camiré, Xavier C Giner, Catherine Brousseau and Jacques J Tremblay

al . 2002 , Koskimies et al . 2003 ). In adults, the role of INSL3 in males is not yet fully understood. INSL3 was found to be involved in bone metabolism ( Ferlin et al . 2008 ) and proposed to act as a germ cell survival factor ( Kawamura et al

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D M Thomas, S D Rogers, K W Ng and J D Best


Corticosteroids have profound effects on bone metabolism, though the underlying mechanisms remain unclear. They are also known to alter glucose metabolism, in part by induction of insulin resistance. To determine whether corticosteroids impair glucose metabolism in bone cells, we have examined the actions of dexamethasone (DEX) on glucose transport and insulin receptor expression using osteoblast-like UMR 106-01 cells. DEX was shown to inhibit basal 2-deoxyglucose uptake by up to 30% in a time- and dose-dependent manner. It inhibited insulin-stimulated glucose transport by 13%. By Northern and Western blot analysis, DEX was shown to stimulate insulin receptor mRNA and protein by up to 5·6-fold, but it had no effect on expression of the glucose transporter GLUT 1 mRNA or protein under basal conditions. However, DEX augmented insulin-stimulated GLUT 1 mRNA and protein levels. By Scatchard analysis of labelled insulin binding, DEX increased insulin receptor number per cell by 54%. Subcellular fractionation and Western blot analysis demonstrated that DEX caused a redistribution of immunoreactive GLUT 1 from plasma membrane to intracellular microsomes, resulting in a 21% decrease in GLUT 1 at the plasma membrane. These data suggest that (i) DEX impairs basal glucose transport by post-translational mechanisms in UMR 106-01 cells, (ii) DEX increases insulin receptor mRNA, protein and insulin binding and (iii) the inhibition of glucose transport by DEX dominates its effects on the insulin receptor. It is possible that DEX inhibition of glucose transport in osteoblasts may contribute to steroid-induced osteoporosis.