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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Main Authors: Kristina Hedbacker, Yi-Hsueh Lu, Olof Dallner, Zhiying Li, Gulya Fayzikhodjaeva, Kıvanç Birsoy, Chiayun Han, Chingwen Yang, Jeffrey M Friedman
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2020-05-01
Series:eLife
Subjects:
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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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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