Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue - Archive ouverte HAL Access content directly
Journal Articles Cell Reports Year : 2016

Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue

Delphine Duteil
Milica Tosic
  • Function : Author
Franziska Lausecker
  • Function : Author
Hatice Z. Nenseth
  • Function : Author
Judith M. Müller
  • Function : Author
Sylvia Urban
  • Function : Author
Dominica Willmann
  • Function : Author
Kerstin Petroll
  • Function : Author
Laura Arrigoni
  • Function : Author
Thomas Manke
  • Function : Author
Jan-Wilhelm Kornfeld
  • Function : Author
Jens C. Bruning
  • Function : Author
Vyacheslav Zagoriy
  • Function : Author
Michael Meret
  • Function : Author
Jörn Dengjel
  • Function : Author
Toufike Kanouni
  • Function : Author
Roland Schüle
  • Function : Author

Abstract

Previous work indicated that lysine-specific demethylase 1 (Lsd1) can positively regulate the oxidative and thermogenic capacities of white and beige adipocytes. Here we investigate the role of Lsd1 in brown adipose tissue (BAT) and find that BAT-selective Lsd1 ablation induces a shift from oxidative to glycolytic metabolism. This shift is associated with downregulation of BAT-specific and upregulation of white adipose tissue (WAT)-selective gene expression. This results in the accumulation of di- and triacylglycerides and culminates in a profound whitening of BAT in aged Lsd1-deficient mice. Further studies show that Lsd1 maintains BAT properties via a dual role. It activates BAT-selective gene expression in concert with the transcription factor Nrf1 and represses WAT-selective genes through recruitment of the CoREST complex. In conclusion, our data uncover Lsd1 as a key regulator of gene expression and metabolic function in BAT.

Dates and versions

hal-03685158 , version 1 (01-06-2022)

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Delphine Duteil, Milica Tosic, Franziska Lausecker, Hatice Z. Nenseth, Judith M. Müller, et al.. Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue. Cell Reports, 2016, 17 (4), pp.1008-1021. ⟨10.1016/j.celrep.2016.09.053⟩. ⟨hal-03685158⟩
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