ID 111601
Title Alternative
腸管および腎臓でのリン代謝におけるNpt2b欠損の影響
Conditional deletion of Npt2b in phosphate transport
Author
Ikuta, Kayo Tokushima University
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
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
Keywords
Intestine
Transcellular transport-paracellular transport
Content Type
Thesis or Dissertation
Description
Background
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.
Methods
In the present study, we made tamoxifen-inducible Npt2b conditional knockout (CKO) mice to analyze systemic Pi metabolism, including intestinal Pi absorption.
Results
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.
Conclusion
These findings indicate that abnormal Pi metabolism may also be involved in tight junction molecules such as Cldns that are affected by Npt2b deficiency.
Journal Title
Clinical and Experimental Nephrology
ISSN
13421751
14377799
NCID
AA11126935
Publisher
Japanese Society of Nephrology|Springer
Volume
22
Issue
3
Start Page
517
End Page
528
Published Date
2017-11-11
Remark
内容要旨・審査要旨・論文本文の公開
本論文は,著者Kayo Ikutaの学位論文として提出され,学位審査・授与の対象となっている。
Rights
© 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
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
ETD
MEXT report number
甲第3139号
Diploma Number
甲栄第248号
Granted Date
2018-03-23
Degree Name
Doctor of Nutritional Science
Grantor
Tokushima University
departments
Medical Sciences