首页    期刊浏览 2024年11月23日 星期六
登录注册

文章基本信息

  • 标题:Expression of Calbindin-D9k, VDR and Cdx-2 Messenger RNA in the Process by Which Fructooligosaccharides Increase Calcium Absorption in Rats
  • 本地全文:下载
  • 作者:Akiko FUKUSHIMA ; Atsutane OHTA ; Kensuke SAKAI
  • 期刊名称:Journal of Nutritional Science and Vitaminology
  • 印刷版ISSN:0301-4800
  • 电子版ISSN:1881-7742
  • 出版年度:2005
  • 卷号:51
  • 期号:6
  • 页码:426-432
  • DOI:10.3177/jnsv.51.426
  • 出版社:Center for Academic Publications Japan
  • 摘要:We have previously shown, through evidence that the expression of calbindinD9k protein shows a dose-dependent change in the intestine, that calbindin-D9k plays a role in the ability of a fructooligosaccharide (FOS) diet to increase calcium absorption. This study shows that the regulation of calbindin-D9k expression occurs at the transcriptional level in a segment-specific manner, decreasing in the proximal intestine and increasing in the colorectal segment. To determine the transcriptional regulation of the FOS diet on calbindinD9k expression, two transcription factors, vitamin D receptor (VDR) and cdx-2, were analyzed during 1 0 d feeding of the FOS diet. The mRNA expression of VDR and cdx-2 was influenced by the FOS diet and showed a segment-specific change. In the proximal small intestine, there was a significant correlation between the changes in both mRNAs ( r =0.69, p <0.01), while the expression of calbindin-D9k correlated neither with VDR nor with cdx2. This means that the transcriptional change induced by the FOS diet was not regulated by VDR and cdx-2. In the colorectal segment, there were significant correlations between gene expressions of calbindin-D9k vs. VDR, r =0.73, p <0.01 and calbindin-D9k vs. cdx-2, r =0.52, p <0.05. These results suggested that both transcription factors, VDR and cdx-2, were involved in the regulation of calbindin-D9k gene expression in the colorectal segment during the process through which the FOS diet enhanced calcium absorption.
  • 关键词:fructooligosaccharides;calbindin-D9k;vitamin D receptor;cdx-2
国家哲学社会科学文献中心版权所有