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Ribas Latre, A. ; Santos, R.B.* ; Fekry, B.* ; Tamim, Y.M.* ; Shivshankar, S.* ; Mohamed, A.M.T.* ; Baumgartner, C.* ; Kwok, C.* ; Gebhardt, C. ; Rivera, A.* ; Gao, Z.* ; Sun, K.* ; Heiker, J.T. ; Snyder, B.E.* ; Kolonin, M.G.* ; Eckel-Mahan, K.L.*

Cellular and physiological circadian mechanisms drive diurnal cell proliferation and expansion of white adipose tissue.

Nat. Commun. 12:3482 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Hyperplastic expansion of white adipose tissue (WAT) relies in part on the proliferation of adipocyte precursor cells residing in the stromal vascular cell fraction (SVF) of WAT. This study reveals a circadian clock- and feeding-induced diurnal pattern of cell proliferation in the SVF of visceral and subcutaneous WAT in vivo, with higher proliferation of visceral adipocyte progenitor cells subsequent to feeding in lean mice. Fasting or loss of rhythmic feeding eliminates this diurnal proliferation, while high fat feeding or genetic disruption of the molecular circadian clock modifies the temporal expression of proliferation genes and impinges on diurnal SVF proliferation in eWAT. Surprisingly, high fat diet reversal, sufficient to reverse elevated SVF proliferation in eWAT, was insufficient in restoring diurnal patterns of SVF proliferation, suggesting that high fat diet induces a sustained disruption of the adipose circadian clock. In conclusion, the circadian clock and feeding simultaneously impart dynamic, regulatory control of adipocyte progenitor proliferation, which may be a critical determinant of adipose tissue expansion and health over time.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter High-fat Diet; Gene-expression; Regulates Adipogenesis; Growth-hormone; Clock Genes; Obesity; Differentiation; Identification; Progenitors; Rhythms
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 12, Heft: 1, Seiten: , Artikelnummer: 3482 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen DK109001
Deutsche Forschungsgemeinschaft
Bovay Foundation
NIH
ACS