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Previous\n                    <jats:italic>in vitro<\/jats:italic>\n                    studies have elucidated basic information about riboflavin transporter RFVT3 encoded by\n                    <jats:italic>SLC52A3<\/jats:italic>\n                    gene. However, the contribution of RFVT3 to the maintenance of riboflavin homeostasis and the significance\n                    <jats:italic>in vivo<\/jats:italic>\n                    remain unclear. Here, we investigated the physiological role of RFVT3 using\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    knockout (\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    \u2212\/\u2212) mice. Most\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    \u2212\/\u2212 mice died with hyperlipidemia and hypoglycemia within 48\u2009hr after birth. The plasma and tissue riboflavin concentrations in\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    \u2212\/\u2212 mice at postnatal day 0 were dramatically lower than those in wild-type (WT) littermates.\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    \u2212\/\u2212 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\n                    <jats:italic>Slc52a3<\/jats:italic>\n                    gene caused neonatal mortality with hyperlipidemia and hypoglycemia owing to riboflavin deficiency.\n                  <\/jats:p>","DOI":"10.1038\/srep27557","type":"journal-article","created":{"date-parts":[[2016,6,8]],"date-time":"2016-06-08T05:48:56Z","timestamp":1465364936000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice"],"prefix":"10.1038","volume":"6","author":[{"given":"Hiroki","family":"Yoshimatsu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atsushi","family":"Yonezawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaori","family":"Yamanishi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiaki","family":"Yao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kumiko","family":"Sugano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shunsaku","family":"Nakagawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoshi","family":"Imai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohiro","family":"Omura","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takayuki","family":"Nakagawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ikuko","family":"Yano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satohiro","family":"Masuda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken-ichi","family":"Inui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuo","family":"Matsubara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2016,6,8]]},"reference":[{"key":"BFsrep27557_CR1","doi-asserted-by":"publisher","first-page":"94","DOI":"10.1016\/j.cbi.2006.04.014","volume":"163","author":"F Depeint","year":"2006","unstructured":"Depeint, F., Bruce, W. 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