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
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Author |
Ikuta, Kayo
Tokushima University
Segawa, Hiroko
Tokushima University
Tokushima University Educator and Researcher Directory
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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
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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
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Keywords | Intestine
Transcellular transport-paracellular transport
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Content Type |
Thesis or Dissertation
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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
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ISSN | 13421751
14377799
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NCID | AA11126935
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Publisher | Japanese Society of Nephrology|Springer
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Volume | 22
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Issue | 3
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Start Page | 517
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End Page | 528
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Published Date | 2017-11-11
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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。 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 |
Rights | © Japanese Society of Nephrology 2017
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EDB ID | |
DOI (Published Version) | |
URL ( Publisher's Version ) | |
FullText File | |
language |
eng
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TextVersion |
ETD
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MEXT report number | 甲第3139号
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Diploma Number | 甲栄第248号
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Granted Date | 2018-03-23
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Degree Name |
Doctor of Nutritional Science
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Grantor |
Tokushima University
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departments |
Medical Sciences
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