Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice

Hiroki Yoshimatsu, Atsushi Yonezawa, Kaori Yamanishi, Yoshiaki Yao, Kumiko Sugano, Shunsaku Nakagawa, Satoshi Imai, Tomohiro Omura, Takayuki Nakagawa, Ikuko Yano, Satohiro Masuda, Ken Ichi Inui, Kazuo Matsubara

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18 Citations (Scopus)


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.

Original languageEnglish
Article number27557
JournalScientific reports
Publication statusPublished - 2016 Jun 8
Externally publishedYes

ASJC Scopus subject areas

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