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Title: Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice.
Authors: Yoshimatsu, Hiroki
Yonezawa, Atsushi  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-8057-6768 (unconfirmed)
Yamanishi, Kaori
Yao, Yoshiaki
Sugano, Kumiko
Nakagawa, Shunsaku  kyouindb  KAKEN_id
Imai, Satoshi  kyouindb  KAKEN_id
Omura, Tomohiro  kyouindb  KAKEN_id
Nakagawa, Takayuki  kyouindb  KAKEN_id
Yano, Ikuko
Masuda, Satohiro
Inui, Ken-ichi
Matsubara, Kazuo  kyouindb  KAKEN_id
Author's alias: 米澤, 淳
松原, 和夫
Issue Date: 8-Jun-2016
Publisher: Springer Nature
Journal title: Scientific reports
Volume: 6
Thesis number: 27557
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.
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/
URI: http://hdl.handle.net/2433/215883
DOI(Published Version): 10.1038/srep27557
PubMed ID: 27272163
Appears in Collections:Journal Articles

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