Limitation of adipose tissue by the number of embryonic progenitor cells
Adipogenesis in adulthood replaces fat cells that turn over and can contribute to the development of obesity. However, the proliferative potential of adipocyte progenitors in vivo is unknown (Faust et al., 1976; Faust et al., 1977; Hirsch and Han, 1969; Johnson and Hirsch, 1972). We addressed this b...
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eLife Sciences Publications Ltd
2020-05-01
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Online Access: | https://elifesciences.org/articles/53074 |
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author | Kristina Hedbacker Yi-Hsueh Lu Olof Dallner Zhiying Li Gulya Fayzikhodjaeva Kıvanç Birsoy Chiayun Han Chingwen Yang Jeffrey M Friedman |
author_facet | Kristina Hedbacker Yi-Hsueh Lu Olof Dallner Zhiying Li Gulya Fayzikhodjaeva Kıvanç Birsoy Chiayun Han Chingwen Yang Jeffrey M Friedman |
author_sort | Kristina Hedbacker |
collection | DOAJ |
description | Adipogenesis in adulthood replaces fat cells that turn over and can contribute to the development of obesity. However, the proliferative potential of adipocyte progenitors in vivo is unknown (Faust et al., 1976; Faust et al., 1977; Hirsch and Han, 1969; Johnson and Hirsch, 1972). We addressed this by injecting labeled wild-type embryonic stem cells into blastocysts derived from lipodystrophic A-ZIP transgenic mice, which have a genetic block in adipogenesis. In the resulting chimeric animals, wild-type ES cells are the only source of mature adipocytes. We found that when chimeric animals were fed a high-fat-diet, animals with low levels of chimerism showed a significantly lower adipose tissue mass than animals with high levels of chimerism. The difference in adipose tissue mass was attributed to variability in the amount of subcutaneous adipose tissue as the amount of visceral fat was independent of the level of chimerism. Our findings thus suggest that proliferative potential of adipocyte precursors is limited and can restrain the development of obesity. |
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id | doaj.art-a2ff7c0eb31940a4b09d0e60faa517fc |
institution | Directory Open Access Journal |
issn | 2050-084X |
language | English |
last_indexed | 2024-04-12T02:43:13Z |
publishDate | 2020-05-01 |
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spelling | doaj.art-a2ff7c0eb31940a4b09d0e60faa517fc2022-12-22T03:51:15ZengeLife Sciences Publications LtdeLife2050-084X2020-05-01910.7554/eLife.53074Limitation of adipose tissue by the number of embryonic progenitor cellsKristina Hedbacker0https://orcid.org/0000-0003-0543-8733Yi-Hsueh Lu1Olof Dallner2https://orcid.org/0000-0001-5614-1716Zhiying Li3https://orcid.org/0000-0002-5586-7782Gulya Fayzikhodjaeva4Kıvanç Birsoy5Chiayun Han6Chingwen Yang7Jeffrey M Friedman8https://orcid.org/0000-0003-2152-0868Laboratory of Molecular Genetics, The Rockefeller University, New York, United States; Howard Hughes Medical Institute, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United States; Howard Hughes Medical Institute, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United States; Laboratory of Metabolic Regulation and Genetics, The Rockefeller University, New York, United StatesGene Targeting Resource Center, The Rockefeller University, New York, United StatesGene Targeting Resource Center, The Rockefeller University, New York, United StatesLaboratory of Molecular Genetics, The Rockefeller University, New York, United States; Howard Hughes Medical Institute, The Rockefeller University, New York, United StatesAdipogenesis in adulthood replaces fat cells that turn over and can contribute to the development of obesity. However, the proliferative potential of adipocyte progenitors in vivo is unknown (Faust et al., 1976; Faust et al., 1977; Hirsch and Han, 1969; Johnson and Hirsch, 1972). We addressed this by injecting labeled wild-type embryonic stem cells into blastocysts derived from lipodystrophic A-ZIP transgenic mice, which have a genetic block in adipogenesis. In the resulting chimeric animals, wild-type ES cells are the only source of mature adipocytes. We found that when chimeric animals were fed a high-fat-diet, animals with low levels of chimerism showed a significantly lower adipose tissue mass than animals with high levels of chimerism. The difference in adipose tissue mass was attributed to variability in the amount of subcutaneous adipose tissue as the amount of visceral fat was independent of the level of chimerism. Our findings thus suggest that proliferative potential of adipocyte precursors is limited and can restrain the development of obesity.https://elifesciences.org/articles/53074adipose tissueobesitymetabolic syndromemetabolismlipodystrophyleptin |
spellingShingle | Kristina Hedbacker Yi-Hsueh Lu Olof Dallner Zhiying Li Gulya Fayzikhodjaeva Kıvanç Birsoy Chiayun Han Chingwen Yang Jeffrey M Friedman Limitation of adipose tissue by the number of embryonic progenitor cells eLife adipose tissue obesity metabolic syndrome metabolism lipodystrophy leptin |
title | Limitation of adipose tissue by the number of embryonic progenitor cells |
title_full | Limitation of adipose tissue by the number of embryonic progenitor cells |
title_fullStr | Limitation of adipose tissue by the number of embryonic progenitor cells |
title_full_unstemmed | Limitation of adipose tissue by the number of embryonic progenitor cells |
title_short | Limitation of adipose tissue by the number of embryonic progenitor cells |
title_sort | limitation of adipose tissue by the number of embryonic progenitor cells |
topic | adipose tissue obesity metabolic syndrome metabolism lipodystrophy leptin |
url | https://elifesciences.org/articles/53074 |
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