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Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice
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Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice
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Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice
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Journal Article
Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice
2016
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 42
/ 42/41
/ 49
/ 64
/ 64/60
/ 82
/ Animals
/ Female
/ Fetuses
/ Humanities and Social Sciences
/ Humans
/ Membrane Transport Proteins - genetics
/ Mice
/ Neonates
/ Placenta
/ Plasma
/ Riboflavin Deficiency - genetics
/ Riboflavin Deficiency - mortality
/ Riboflavin Deficiency - pathology
/ Science
