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|Title:||1,25-Dihydroxyvitamin D3-induced intestinal calcium transport is impaired in β-globin knockout thalassemic mice|
|Keywords:||Biochemistry, Genetics and Molecular Biology;Medicine|
|Citation:||Cell Biochemistry and Function. Vol.31, No.8 (2013), 685-691|
|Abstract:||Besides being a common haematological disorder caused by a reduction in β-globin production, β-thalassemia has been reported to impair body calcium homeostasis, leading to massive bone loss and increased fracture risk. Here, we demonstrated that heterozygous β-globin knockout thalassemic mice had a lower rate of duodenal calcium absorption compared with the wild-type littermates, whereas the epithelial electrical parameters, including transepithelial resistance, were not affected, suggesting no change in the epithelial integrity and permeability. Daily subcutaneous injection of 1μgkg-1 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] for 3days enhanced the duodenal calcium absorption in wild-type, but not in thalassemic mice. Although β-thalassemia increased the mRNA level of divalent metal transporter-1, an iron transporter in the duodenum, it had no effect on the transcripts of ferroportin-1 or the principal calcium transporters. In conclusion, β-thalassemia impaired the 1,25(OH)2D3-dependent intestinal calcium absorption at the post-transcriptional level, which, in turn, contributed to the dysregulation of body calcium metabolism and β-thalassemia-induced osteopenia. © 2013 John Wiley & Sons, Ltd.|
|Appears in Collections:||Scopus 2011-2015|
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