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作 者:郑维[1] 康红[2] 杨进福[3] 李洋[1] 叶俊[1]
机构地区:[1]湖南省人民医院普外二科,湖南长沙410005 [2]湖南省人民医院急诊科 [3]中南大学湘雅二医院胸外科
出 处:《中国医师杂志》2008年第9期1179-1182,共4页Journal of Chinese Physician
摘 要:目的探讨小鼠肾脏Calbindin.D28k(CaBP.D28k)在钙代谢中的作用。方法构建维生素D受体(Vitamin D Receptor,VDR)/calbjndin.D28k双基因剔除小鼠模型,在普通及高钙饮食下,检测小鼠体重、摄食量、血尿参数值、下肢骨的长度、密度以及胫骨切片组织学染色等。结果普通饮食下,VDR(-/-)/CaBP—D28k(-/-)小鼠发育更迟缓,体重比VDR(-/-)小鼠轻42%,尿钙的分泌更高,发展为更严重的佝偻病骨表型,表现为骨密度较低和骨小梁区生长板变形更多。高钙饮食下,VDR(-/-)及VDR(-/-)/CaBP-1)28k(-/-)小鼠的血钙离子正常,VDR(-/-)/CaBP—D28k(-/-)小鼠的骨骼异常未得到完全纠正。结论CaBP-D28k对骨质的生长发育起了重要作用,它对钙代谢的作用大都可被CaBP-D9k补偿。Objective To investigate the role of Calbindin-D28k in the kidney on calcium metabolism. Methods VDR/CaBP- D28k double knockout (KO) mice was made. Body weight, diet intake and serum, urinary parameters and length, density of the long bones, histological staining of the tibia of WT, CaBP-D28( -/- ) , VDR( -/- ) and VDR( -/- )/CaBP-D28k( -/- ) mice were de- termined on regular and high Ca-Lae diet. Results On a regular diet, the double KO mice were growth-retarded more and smaller than VDR KO mice. Compared with VDR KO mice, the double KO mice had higher urinary calcium excretion and rachitie skeletal phenotype, which were manifested with higher serum parathyroid hormone levels, lower bone mineral density, and more distorted growth plate with more osteoid formation in the trabecular region. On high calcium and high lactose diet, blood-ionized calcium levels were normal in both VDR KO and the double KO mice. However, in contrast to VDR KO mice, the skeletal abnormalities were not completely corrected in the double KO mice. Conclusion These results directly demonstrate that CaBP-D28k plays a critical role in maintaining calcium homeostasis and skeletal mineralization and suggest that its calcemic role can be mostly compensated by CaBP-D9k.
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