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Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells

Vitamin A has preventive effects on obesity. All-trans retinoic acid (ATRA), the active form of vitamin A, inhibits lipid accumulation in 3T3-L1 cells in an experimental adipogenesis model. We found that ATRA suppressed up-regulation of the amino acid transporter, Asct2, in adipogenerating 3T3-L1 ce...

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Autores principales: Takahashi, Katsuhiko, Uchida, Natsumi, Kitanaka, Chisato, Sagara, Chiaki, Imai, Masahiko, Takahashi, Noriko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511454/
https://www.ncbi.nlm.nih.gov/pubmed/26236584
http://dx.doi.org/10.1016/j.fob.2015.06.012
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author Takahashi, Katsuhiko
Uchida, Natsumi
Kitanaka, Chisato
Sagara, Chiaki
Imai, Masahiko
Takahashi, Noriko
author_facet Takahashi, Katsuhiko
Uchida, Natsumi
Kitanaka, Chisato
Sagara, Chiaki
Imai, Masahiko
Takahashi, Noriko
author_sort Takahashi, Katsuhiko
collection PubMed
description Vitamin A has preventive effects on obesity. All-trans retinoic acid (ATRA), the active form of vitamin A, inhibits lipid accumulation in 3T3-L1 cells in an experimental adipogenesis model. We found that ATRA suppressed up-regulation of the amino acid transporter, Asct2, in adipogenerating 3T3-L1 cells. We observed that Asct2 was up-regulated at 1 day after adipogenesis stimuli. The Asct2 inhibitor l-γ-glutamyl-p-nitroanilide (GPNA) decreased lipid accumulation. Glutamine-free conditions also suppressed adipogenesis. Suppression of adipogenesis by ATRA may be through Asct2 reduction. These results indicate that Asct2 could be a target for obesity prevention and treatment.
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spelling pubmed-45114542015-08-01 Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells Takahashi, Katsuhiko Uchida, Natsumi Kitanaka, Chisato Sagara, Chiaki Imai, Masahiko Takahashi, Noriko FEBS Open Bio Research article Vitamin A has preventive effects on obesity. All-trans retinoic acid (ATRA), the active form of vitamin A, inhibits lipid accumulation in 3T3-L1 cells in an experimental adipogenesis model. We found that ATRA suppressed up-regulation of the amino acid transporter, Asct2, in adipogenerating 3T3-L1 cells. We observed that Asct2 was up-regulated at 1 day after adipogenesis stimuli. The Asct2 inhibitor l-γ-glutamyl-p-nitroanilide (GPNA) decreased lipid accumulation. Glutamine-free conditions also suppressed adipogenesis. Suppression of adipogenesis by ATRA may be through Asct2 reduction. These results indicate that Asct2 could be a target for obesity prevention and treatment. Elsevier 2015-07-02 /pmc/articles/PMC4511454/ /pubmed/26236584 http://dx.doi.org/10.1016/j.fob.2015.06.012 Text en © 2015 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research article
Takahashi, Katsuhiko
Uchida, Natsumi
Kitanaka, Chisato
Sagara, Chiaki
Imai, Masahiko
Takahashi, Noriko
Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title_full Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title_fullStr Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title_full_unstemmed Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title_short Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells
title_sort inhibition of asct2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3t3-l1 cells
topic Research article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511454/
https://www.ncbi.nlm.nih.gov/pubmed/26236584
http://dx.doi.org/10.1016/j.fob.2015.06.012
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