Conditional deletion of Npt2b in phosphate transport
Ikuta, Kayo Tokushima University
Segawa, Hiroko Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Sasaki, Shohei Tokushima University
Hanazaki, Ai Tokushima University
Fujii, Toru Tokushima University
Kushi, Aoi Tokushima University
Kawabata, Yuka Tokushima University
Kirino, Ruri Tokushima University
Sasaki, Sumire Tokushima University
Noguchi, Miwa Tokushima University
Kaneko, Ichiro Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Ueda, Otoya Chugai Pharmaceutical
Wada, Naoko A. Chugai Pharmaceutical
Tateishi, Hiromi Chugai Research Institute for Medical Science
Kakefuda, Mami Chugai Research Institute for Medical Science
Kawase, Yosuke Chugai Research Institute for Medical Science
Ohtomo, Shuichi Chugai Pharmaceutical
Ichida, Yasuhiro Chugai Pharmaceutical
Maeda, Akira Chugai Pharmaceutical
Jishage, Kou-ichi Chugai Pharmaceutical|Chugai Research Institute for Medical Science
Horiba, Naoshi Chugai Pharmaceutical
Transcellular transport-paracellular transport
Thesis or Dissertation
Hyperphosphatemia is common in chronic kidney disease and is associated with morbidity and mortality. The intestinal Na+-dependent phosphate transporter Npt2b is thought to be an important molecular target for the prevention of hyperphosphatemia. The role of Npt2b in the net absorption of inorganic phosphate (Pi), however, is controversial.
In the present study, we made tamoxifen-inducible Npt2b conditional knockout (CKO) mice to analyze systemic Pi metabolism, including intestinal Pi absorption.
Although the Na+-dependent Pi transport in brush-border membrane vesicle uptake levels were significantly decreased in the distal intestine of Npt2b CKO mice compared with control mice, plasma Pi and fecal Pi excretion levels were not significantly different. Data obtained using the intestinal loop technique showed that Pi uptake in Npt2b CKO mice was not affected at a Pi concentration of 4 mM, which is considered the typical luminal Pi concentration after meals in mice. Claudin, which may be involved in paracellular pathways, as well as claudin-2, 12, and 15 protein levels were significantly decreased in the Npt2b CKO mice. Thus, Npt2b deficiency did not affect Pi absorption within the range of Pi concentrations that normally occurs after meals.
These findings indicate that abnormal Pi metabolism may also be involved in tight junction molecules such as Cldns that are affected by Npt2b deficiency.
Clinical and Experimental Nephrology
Japanese Society of Nephrology|Springer
© Japanese Society of Nephrology 2017
This is a post-peer-review, pre-copyedit version of an article published in Clinical and Experimental Nephrology.
The final publication is available at Springer via https://doi.org/10.1007/s10157-017-1497-3
|DOI (Published Version)|
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|MEXT report number||
Doctor of Nutritional Science