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Huang, J.* ; Linares, J.F.* ; Duran, A.* ; Xia, W.* ; Saltiel, A.R.* ; Müller, T.D. ; Diaz-Meco, M.T.* ; Moscat, J.*

NBR1 is a critical step in the repression of thermogenesis of p62-deficient adipocytes through PPARγ.

Nat. Commun. 12:2876 (2021)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Activation of non-shivering thermogenesis is considered a promising approach to lower body weight in obesity. p62 deficiency in adipocytes reduces systemic energy expenditure but its role in sustaining mitochondrial function and thermogenesis remains unresolved. NBR1 shares a remarkable structural similarity with p62 and can interact with p62 through their respective PB1 domains. However, the physiological relevance of NBR1 in metabolism, as compared to that of p62, was not clear. Here we show that whole-body and adipocyte-specific ablation of NBR1 reverts the obesity phenotype induced by p62 deficiency by restoring global energy expenditure and thermogenesis in brown adipose tissue. Impaired adrenergic-induced browning of p62-deficient adipocytes is rescued by NBR1 inactivation, unveiling a negative role of NBR1 in thermogenesis under conditions of p62 loss. We demonstrate that upon p62 inactivation, NBR1 represses the activity of PPARγ, establishing an unexplored p62/NBR1-mediated paradigm in adipocyte thermogenesis that is critical for the control of obesity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Brown Adipose-tissue; Signaling Adapter; Mice Deficient; Fat; P62; Cell; Metabolism; Autophagy; Obesity; Inflammation
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 12, Heft: 1, Seiten: , Artikelnummer: 2876 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Förderungen NCI NIH HHS
NIDDK NIH HHS