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dc.contributor.author | Yoshimatsu, Hiroki | en |
dc.contributor.author | Yonezawa, Atsushi | en |
dc.contributor.author | Yamanishi, Kaori | en |
dc.contributor.author | Yao, Yoshiaki | en |
dc.contributor.author | Sugano, Kumiko | en |
dc.contributor.author | Nakagawa, Shunsaku | en |
dc.contributor.author | Imai, Satoshi | en |
dc.contributor.author | Omura, Tomohiro | en |
dc.contributor.author | Nakagawa, Takayuki | en |
dc.contributor.author | Yano, Ikuko | en |
dc.contributor.author | Masuda, Satohiro | en |
dc.contributor.author | Inui, Ken-ichi | en |
dc.contributor.author | Matsubara, Kazuo | en |
dc.contributor.alternative | 米澤, 淳 | ja |
dc.contributor.alternative | 松原, 和夫 | ja |
dc.contributor.transcription | ヨネザワ, アツシ | ja |
dc.contributor.transcription | マツバラ, カズオ | ja |
dc.date.accessioned | 2016-07-08T02:02:47Z | - |
dc.date.available | 2016-07-08T02:02:47Z | - |
dc.date.issued | 2016-06-08 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/2433/215883 | - |
dc.description.abstract | Homeostasis of riboflavin should be maintained by transporters. Previous in vitro studies have elucidated basic information about riboflavin transporter RFVT3 encoded by SLC52A3 gene. However, the contribution of RFVT3 to the maintenance of riboflavin homeostasis and the significance in vivo remain unclear. Here, we investigated the physiological role of RFVT3 using Slc52a3 knockout (Slc52a3−/−) mice. Most Slc52a3−/− mice died with hyperlipidemia and hypoglycemia within 48 hr after birth. The plasma and tissue riboflavin concentrations in Slc52a3−/− mice at postnatal day 0 were dramatically lower than those in wild-type (WT) littermates. Slc52a3−/− fetuses showed a lower capacity of placental riboflavin transport compared with WT fetuses. Riboflavin supplement during pregnancy and after birth reduced neonatal death and metabolic disorders. To our knowledge, this is the first report to indicate that Rfvt3 contributes to placental riboflavin transport, and that disruption of Slc52a3 gene caused neonatal mortality with hyperlipidemia and hypoglycemia owing to riboflavin deficiency. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Springer Nature | en |
dc.rights | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ | en |
dc.title | Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice. | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Scientific reports | en |
dc.identifier.volume | 6 | - |
dc.relation.doi | 10.1038/srep27557 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | 27557 | - |
dc.identifier.pmid | 27272163 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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