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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
著者
生田, かよ 徳島大学大学院栄養生命科学教育部(人間栄養科学専攻)
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
キーワード
Intestine
Transcellular transport-paracellular transport
資料タイプ
学位論文
抄録
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.
掲載誌名
Clinical and Experimental Nephrology
ISSN
13421751
14377799
cat書誌ID
AA11126935
出版者
Japanese Society of Nephrology|Springer
22
3
開始ページ
517
終了ページ
528
発行日
2017-11-11
備考
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。
権利情報
© 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
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
博士論文全文を含む
文科省報告番号
甲第3139号
学位記番号
甲栄第248号
学位授与年月日
2018-03-23
学位名
博士(栄養学)
学位授与機関
徳島大学
部局
医学系