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Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching
Adapting the energy metabolism state to changing bioenergetic demands is essential for mammalian development accompanying massive cell proliferation and cell differentiation. However, it remains unclear how developing embryos meet the changing bioenergetic demands during the chorioallantoic branchin...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Ltd
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5278628/ https://www.ncbi.nlm.nih.gov/pubmed/28049690 http://dx.doi.org/10.1242/dev.138545 |
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author | Miyazawa, Hidenobu Yamaguchi, Yoshifumi Sugiura, Yuki Honda, Kurara Kondo, Koki Matsuda, Fumio Yamamoto, Takehiro Suematsu, Makoto Miura, Masayuki |
author_facet | Miyazawa, Hidenobu Yamaguchi, Yoshifumi Sugiura, Yuki Honda, Kurara Kondo, Koki Matsuda, Fumio Yamamoto, Takehiro Suematsu, Makoto Miura, Masayuki |
author_sort | Miyazawa, Hidenobu |
collection | PubMed |
description | Adapting the energy metabolism state to changing bioenergetic demands is essential for mammalian development accompanying massive cell proliferation and cell differentiation. However, it remains unclear how developing embryos meet the changing bioenergetic demands during the chorioallantoic branching (CB) stage, when the maternal-fetal exchange of gases and nutrients is promoted. In this study, using metabolome analysis with mass-labeled glucose, we found that developing embryos redirected glucose carbon flow into the pentose phosphate pathway via suppression of the key glycolytic enzymes PFK-1 and aldolase during CB. Concomitantly, embryos exhibited an increase in lactate pool size and in the fractional contribution of glycolysis to lactate biosynthesis. Imaging mass spectrometry visualized lactate-rich tissues, such as the dorsal or posterior neural tube, somites and head mesenchyme. Furthermore, we found that the heterochronic gene Lin28a could act as a regulator of the metabolic changes observed during CB. Perturbation of glucose metabolism rewiring by suppressing Lin28a downregulation resulted in perinatal lethality. Thus, our work demonstrates that developing embryos rewire glucose metabolism following CB for normal development. |
format | Online Article Text |
id | pubmed-5278628 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The Company of Biologists Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-52786282017-03-01 Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching Miyazawa, Hidenobu Yamaguchi, Yoshifumi Sugiura, Yuki Honda, Kurara Kondo, Koki Matsuda, Fumio Yamamoto, Takehiro Suematsu, Makoto Miura, Masayuki Development Research Article Adapting the energy metabolism state to changing bioenergetic demands is essential for mammalian development accompanying massive cell proliferation and cell differentiation. However, it remains unclear how developing embryos meet the changing bioenergetic demands during the chorioallantoic branching (CB) stage, when the maternal-fetal exchange of gases and nutrients is promoted. In this study, using metabolome analysis with mass-labeled glucose, we found that developing embryos redirected glucose carbon flow into the pentose phosphate pathway via suppression of the key glycolytic enzymes PFK-1 and aldolase during CB. Concomitantly, embryos exhibited an increase in lactate pool size and in the fractional contribution of glycolysis to lactate biosynthesis. Imaging mass spectrometry visualized lactate-rich tissues, such as the dorsal or posterior neural tube, somites and head mesenchyme. Furthermore, we found that the heterochronic gene Lin28a could act as a regulator of the metabolic changes observed during CB. Perturbation of glucose metabolism rewiring by suppressing Lin28a downregulation resulted in perinatal lethality. Thus, our work demonstrates that developing embryos rewire glucose metabolism following CB for normal development. The Company of Biologists Ltd 2017-01-01 /pmc/articles/PMC5278628/ /pubmed/28049690 http://dx.doi.org/10.1242/dev.138545 Text en © 2017. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by/3.0This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article Miyazawa, Hidenobu Yamaguchi, Yoshifumi Sugiura, Yuki Honda, Kurara Kondo, Koki Matsuda, Fumio Yamamoto, Takehiro Suematsu, Makoto Miura, Masayuki Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title | Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title_full | Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title_fullStr | Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title_full_unstemmed | Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title_short | Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching |
title_sort | rewiring of embryonic glucose metabolism via suppression of pfk-1 and aldolase during mouse chorioallantoic branching |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5278628/ https://www.ncbi.nlm.nih.gov/pubmed/28049690 http://dx.doi.org/10.1242/dev.138545 |
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