Involvement of riboflavin transporter RFVT2/Slc52a2 in hepatic homeostasis of riboflavin in mice

Yao, Yoshiaki; Yonezawa, Atsushi; Yoshimatsu, Hiroki; Omura, Tomohiro; Masuda, Satohiro; Matsubara, Kazuo

doi:10.1016/j.ejphar.2013.07.042

Cited by 14 publications

(8 citation statements)

References 23 publications

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“…However, the contribution of each RFVT in the human hepatic homeostasis of Rf has not yet been fully clarified, apart from data reported in “The human protein Atlas database” suggesting the prevalence of RFVT2. Similar conclusions have been also reported in the mouse model [ 38 ].…”

Section: Rf Absorption and Cell Deliverysupporting

confidence: 91%

“…Riboflavin transporters, RFVT2/ Slc52a2 and RFVT3/ Slc52a3 , have been identified in rodents. mRFVT2 is the orthologue of both hRFVT1 and hRFVT2 and it is involved in hepatic homeostasis of Rf in mice [ 38 ]. mRFVT3 is the orthologue of hRFVT3 [ 190 ] and it has been shown to be the main transporter involved in carrier-mediated RF uptake in the native mouse small and large intestine [ 191 ].…”

Section: Model Organisms To Study Flavin Homeostasis Alterationsmentioning

confidence: 99%

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Development of Novel Experimental Models to Study Flavoproteome Alterations in Human Neuromuscular Diseases: The Effect of Rf Therapy

Tolomeo

Nisco

Leone

et al. 2020

IJMS

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Inborn errors of Riboflavin (Rf) transport and metabolism have been recently related to severe human neuromuscular disorders, as resulting in profound alteration of human flavoproteome and, therefore, of cellular bioenergetics. This explains why the interest in studying the “flavin world”, a topic which has not been intensively investigated before, has increased much over the last few years. This also prompts basic questions concerning how Rf transporters and FAD (flavin adenine dinucleotide) -forming enzymes work in humans, and how they can create a coordinated network ensuring the maintenance of intracellular flavoproteome. The concept of a coordinated cellular “flavin network”, introduced long ago studying humans suffering for Multiple Acyl-CoA Dehydrogenase Deficiency (MADD), has been, later on, addressed in model organisms and more recently in cell models. In the frame of the underlying relevance of a correct supply of Rf in humans and of a better understanding of the molecular rationale of Rf therapy in patients, this review wants to deal with theories and existing experimental models in the aim to potentiate possible therapeutic interventions in Rf-related neuromuscular diseases.

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Section: Rf Absorption and Cell Deliverysupporting

confidence: 91%

Section: Model Organisms To Study Flavin Homeostasis Alterationsmentioning

confidence: 99%

Development of Novel Experimental Models to Study Flavoproteome Alterations in Human Neuromuscular Diseases: The Effect of Rf Therapy

Tolomeo

Nisco

Leone

et al. 2020

IJMS

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“…41,55 Riboflavin exists in plasma typically between 1 and 100 nM. 56,57 Furthermore, DNA (6) 410 where I is the fluence at the implantation site, γ ex is the tissue 411 extinction coefficient at the excitation wavelength, and d is 412 distance through tissue. The fluorescence intensity of the 413 hydrogel at the implantation site is described by i k j j j j y…”

Section: Riboflavin As a Model Analyte For Chemical Sensing Inmentioning

confidence: 99%

Implanted Nanosensors in Marine Organisms for Physiological Biologging: Design, Feasibility, and Species Variability

et al. 2018

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In recent decades, biologists have sought to tag animals with various sensors to study aspects of their behavior otherwise inaccessible from controlled laboratory experiments. Despite this, chemical information, both environmental and physiological, remains challenging to collect despite its tremendous potential to elucidate a wide range of animal behaviors. In this work, we explore the design, feasibility, and data collection constraints of implantable, near-infrared fluorescent nanosensors based on DNA-wrapped single-wall carbon nanotubes (SWNT) embedded within a biocompatible poly(ethylene glycol) diacrylate (PEGDA) hydrogel. These sensors are enabled by Corona Phase Molecular Recognition (CoPhMoRe) to provide selective chemical detection for marine organism biologging. Riboflavin, a key nutrient in oxidative phosphorylation, is utilized as a model analyte in in vitro and ex vivo tissue measurements. Nine species of bony fish, sharks, eels, and turtles were utilized on site atOceanografc in Valencia, Spain to investigate sensor design parameters, including implantation depth, sensor imaging and detection limits, fluence, and stability, as well as acute and long-term biocompatibility. Hydrogels were implanted subcutaneously and imaged using a customized, field-portable Raspberry Pi camera system. Hydrogels could be detected up to depths of 7 mm in the skin and muscle tissue of deceased teleost fish (Sparus aurata and Stenotomus chrysops) and a deceased catshark (Galeus melastomus). The

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“…The glutaric acid levels in urine samples were determined using a gas chromatography mass spectrometer (GC/MS) at Shimadzu Techno-Research Inc. The concentrations of riboflavin, FMN, and FAD in plasma and tissue samples were measured by HPLC as described previously 37 . Plasma acylcarnitine levels were measured by Electrospray tandem mass spectrometry (ESI-MS/MS) at Shimadzu Techno-Research Inc. 38 with some modifications.…”

Section: Methodsmentioning

confidence: 99%

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

Yoshimatsu

Yonezawa

Yamanishi

et al. 2016

Sci Rep

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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.

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Involvement of riboflavin transporter RFVT2/Slc52a2 in hepatic homeostasis of riboflavin in mice

Cited by 14 publications

References 23 publications

Development of Novel Experimental Models to Study Flavoproteome Alterations in Human Neuromuscular Diseases: The Effect of Rf Therapy

Development of Novel Experimental Models to Study Flavoproteome Alterations in Human Neuromuscular Diseases: The Effect of Rf Therapy

Implanted Nanosensors in Marine Organisms for Physiological Biologging: Design, Feasibility, and Species Variability

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

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