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Reduced subcutaneous adipogenesis in human hypertrophic obesity is linked to senescent precursor cells

Journal article
Authors Birgit Gustafson
Annika Nerstedt
Ulf Smith
Published in Nature Communications
Volume 10
ISSN 2041-1723
Publication year 2019
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Keywords adipose-tissue, cellular senescence, adipocyte lineage, commitment, disease, activation, mechanisms, wisp2, white, risk
Subject categories Clinical Medicine


Inappropriate expansion of the adipose cells in the subcutaneous adipose tissue (SAT) is a characteristic of hypertrophic obesity and of individuals with genetic predisposition for T2D (first-degree relatives; FDR). It is associated with insulin resistance, a dysfunctional, adipose tissue and reduced adipogenesis. We examined the regulation of adipogenesis in human SAT precursor cells and found ZNF521 to be a critical regulator of early adipogenic commitment and precursor cells leaving the cell cycle. However, neither altered upstream signalling nor lack of SAT progenitor cells could explain the reduced adipogenesis in hypertrophic obesity. Instead, we show that progenitor cells undergoing poor differentiation are characterized by senescence, inability to suppress p53/P16(INK4) and secretion of factors reducing adipogenesis in non-senescent cells. We found aging, FDR and established T2D to be associated with increased progenitor cell senescence, reduced adipogenesis and hypertrophic expansion of the SAT adipose cells.

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