All Phenotypes Slc52a3<tm2a(KOMP)Wtsi> MGI Mouse

premature death ( J:236029 )

• any remaining mice die before P60

neonatal lethality, incomplete penetrance ( J:236029 )

• most newborns are alive for more than 8 hr but only ~40% survive to P1

• however, under riboflavin supplementation during pregnancy and after birth, neonatal survival is comparable to that of wild-type controls

postnatal lethality, incomplete penetrance ( J:236029 )

• most mice die suddenly within 48 hr after birth

• less than 20% of mice survive to P2 and approximately half of these die by weaning

• however, under riboflavin supplementation during pregnancy and after birth, survival to weaning age is comparable to that of wild-type controls

decreased birth weight ( J:236029 )

• at P0, body weights are significantly lower than those in wild-type controls

• however, riboflavin-supplemented P0 pups show significantly increased body weight relative to untreated pups

decreased body weight ( J:236029 )

• under riboflavin supplementation during pregnancy and after birth, body weight around P20 is lower than that of wild-type controls

decreased fetal weight ( J:236029 )

• at E16.5, fetal weight is significantly lower than that in wild-type controls (594 +/- 22 versus 722 +/- 22 mg)

• however, fetal to placental weight ratio is not significantly altered

decreased placenta weight ( J:236029 )

• at E16.5, placental weight is significantly lower than that in wild-type controls (102 +/- 2 versus 114 +/- 5 mg)

abnormal placental transport ( J:236029 )

• upon i.v. administration of [3H]riboflavin to pregnant dams at E16.5, placental [3H]riboflavin transport capacity (adjusted by placental weight) is significantly lower than that in wild-type fetuses

• however, placental transport of D-[U-14C]glucose is not significantly altered

decreased food intake ( J:236029 )

• maternal milk ingestion is lower than that in wild-type pups

homeostasis/metabolism phenotype ( J:236029 )

N	• at P0, blood lactate levels are similar to those in wild-type pups

increased circulating carnitine level ( J:236029 )

• at P0, plasma levels of several acylcarnitines (C4, C5, and C14) are significantly increased relative to those in wild-type controls

• however, acylcarnitine levels are significantly improved (decreased) by riboflavin supplementation during pregnancy

hypoglycemia ( J:236029 )

• at P0, blood glucose levels are undetectable in most pups (<20 mg/dL), unlike in wild-type pups

• P0 blood glucose levels are significantly increased by riboflavin supplementation during pregnancy

• under riboflavin supplementation during pregnancy and after birth, 3-week-old riboflavin-treated mice show blood glucose levels similar to those in wild-type controls; however, after riboflavin removal from 3 to 5 weeks after birth, 5-week-old untreated mice show significantly lower blood glucose levels than wild-type controls

abnormal lipid homeostasis ( J:236029 )

• at P0, pups exhibit a disorder in fatty acid metabolism, including increased levels of plasma acylcarnitines and urinary glutaric acid

• however, fatty acid metabolism is significantly improved by riboflavin supplementation of dams during pregnancy

decreased fatty acid beta-oxidation ( J:236029 )

hyperlipidemia ( J:236029 )

glutaricadicuria ( J:236029 )

• at P0, urinary levels of glutaric acid, a marker for fatty acid metabolism disorder, are significantly increased

abnormal vitamin homeostasis ( J:236029 )

• at P0, plasma levels of flavin adenine dinucleotide (FAD), but not flavin mononucleotide (FMN), are significantly reduced relative to those in wild-type pups

• tissue levels of FAD are significantly decreased in the brain, lung, heart, liver and kidney relative to those in wild-type pups

• tissue levels of FMN are significantly decreased in the brain, lung, liver and kidney, but not in heart, relative to those in wild-type pups

• following riboflavin supplementation of dams during pregnancy, FAD levels are significantly increased in all tissues analyzed relative to those in untreated newborn pups

• following riboflavin supplementation of dams during pregnancy, FMN levels are significantly increased in the brain, heart, and kidney, but not in the lung or liver, relative to those in untreated newborn pups

abnormal vitamin level ( J:236029 )

• at P0, plasma riboflavin (water-soluble vitamin B2) levels are dramatically lower than those in wild-type pups

• at P0, tissue levels of riboflavin are significantly decreased in the brain, lung, heart, liver and kidney relative to those in wild-type pups

• upon i.v. administration of [3H]riboflavin to pregnant dams at E16.5, [3H]riboflavin levels are significantly lower than those in wild-type fetuses

• however, following riboflavin supplementation of dams during pregnancy, P0 pups show significantly increased plasma riboflavin levels relative to untreated pups

decreased fatty acid beta-oxidation ( J:236029 )

glutaricadicuria ( J:236029 )

• at P0, urinary levels of glutaric acid, a marker for fatty acid metabolism disorder, are significantly increased

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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