首页> 外文期刊>The Journal of Reproduction and Development >Dietary Calcium and 1,25-Dihydroxyvitamin D-3 Regulate Transcription of Calcium Transporter Genes in Calbindin-D9k Knockout Mice
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Dietary Calcium and 1,25-Dihydroxyvitamin D-3 Regulate Transcription of Calcium Transporter Genes in Calbindin-D9k Knockout Mice

机译:饮食中的钙和1,25-二羟基维生素D-3调节Calbindin-D9k基因敲除小鼠中钙转运蛋白基因的转录。

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摘要

The effect(s) of oral calcium and vitamin D-3 were examined on the expression of duodenal and renal active calcium transport genes, i.e., calbindin-D9k (CaBP-9k) and calbindin-D28k (CaBP-28k), transient receptor potential cation channels (TRPV5 and TRPV6), Na+/Ca2+ exchanger 1 (NCX1) and plasma membrane calcium ATPase 1b (PMCA1b), in CaBP-9k KO mice. Wild-type (WT) and KO mice were provided with calcium and vitamin D-3-deficient diets for 10 weeks. The deficient diet significantly decreased body weights compared with the normal diet groups. The serum calcium concentration of the WT mice was decreased by the deficient diet but was unchanged in the KO mice. The deficient diet significantly increased duodenal transcription of CaBP-9k and TRPV6 in the WT mice, but no alteration was observed in the KO mice. In the kidney, the deficient diet significantly increased renal transcripts of CaBP-9k, TRPV6, PMCA1b, CaBP-28k and TRPV5 in the WT mice but did not alter calcium-relating genes in the KO mice. Two potential mediators of calcium-processing genes, vitamin D receptor (VDR) and parathyroid hormone receptor (PTHR), have been suggested to be useful for elucidating these differential regulations in the calcium-related genes of the KO mice. Expression of VDR was not significantly affected by diet or the KO mutation. Renal PTHR mRNA levels were reduced by the diet, and reduced expression was also seen in the KO mice given the normal diet. Taken together, these results suggest that the active calcium transporting genes in KO mice may have resistance to the deficiency diet of calcium and vitamin D-3.
机译:检查了口服钙和维生素D-3对十二指肠和肾脏活性钙转运基因即calbindin-D9k(CaBP-9k)和calbindin-D28k(CaBP-28k),瞬时受体电位的表达的影响阳离子通道(TRPV5和TRPV6),Na + / Ca2 +交换子1(NCX1)和质膜钙ATPase 1b(PMCA1b),位于CaBP-9k KO小鼠中。向野生型(WT)和KO小鼠提供钙和维生素D-3缺乏饮食,持续10周。与正常饮食组相比,饮食不足显着降低了体重。饮食不足会降低WT小鼠的血清钙浓度,但在KO小鼠中则保持不变。饮食不足在WT小鼠中显着增加CaBP-9k和TRPV6的十二指肠转录,但在KO小鼠中未观察到改变。在肾脏中,饮食不足会显着增加WT小鼠中CaBP-9k,TRPV6,PMCA1b,CaBP-28k和TRPV5的肾转录,但不会改变KO小鼠中与钙有关的基因。已经提出了钙加工基因的两种潜在介体,维生素D受体(VDR)和甲状旁腺激素受体(PTHR),对于阐明KO小鼠钙相关基因中的这些差异性调控很有用。饮食或KO突变对VDR的表达没有显着影响。饮食降低了肾脏的PTHR mRNA水平,在正常饮食的KO小鼠中也观察到了表达降低。综上所述,这些结果表明KO小鼠中的活性钙转运基因可能对缺乏钙和维生素D-3的饮食具有抗性。

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