STAT5 is required for lipid breakdown and beta-adrenergic responsiveness of brown adipose tissue.
Adipocytes
/ metabolism
Adipose Tissue, Brown
/ metabolism
Adipose Tissue, White
/ metabolism
Animals
Cold-Shock Response
/ physiology
Energy Metabolism
Female
Lipid Metabolism
/ physiology
Lipids
/ physiology
Lipolysis
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondria
/ metabolism
Obesity
/ metabolism
Receptors, Adrenergic, beta
/ metabolism
STAT5 Transcription Factor
/ metabolism
Thermogenesis
/ physiology
JAK-STAT
Temperature maintenance
Thermogenesis
β-adrenergic signalling
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
22
11
2019
revised:
10
05
2020
accepted:
23
05
2020
pubmed:
31
5
2020
medline:
9
7
2021
entrez:
31
5
2020
Statut:
ppublish
Résumé
Increasing energy expenditure through activation of brown adipose tissue (BAT) thermogenesis is an attractive approach to counteract obesity. It is therefore essential to understand the molecular mechanisms that control BAT functions. Until now several members of the Janus kinase (JAK) - signal transducer and activator of transcription (STAT) pathway have been implicated as being relevant for BAT physiology. However, whether the STAT family member STAT5 is important for the thermogenic property of adipose tissues is unknown. Therefore, we have investigated the role of STAT5 in thermogenic fat in this paper. We performed metabolic and molecular analyses using mice that harbor an adipocyte-specific deletion of Stat5a/b alleles. We found that STAT5 is necessary for acute cold-induced temperature maintenance and the induction of lipid mobilization in BAT following β We conclude that STAT5 is essential for the functionality and the β-adrenergic responsiveness of thermogenic adipose tissue.
Identifiants
pubmed: 32473405
pii: S2212-8778(20)30100-9
doi: 10.1016/j.molmet.2020.101026
pmc: PMC7322099
pii:
doi:
Substances chimiques
Lipids
0
Receptors, Adrenergic, beta
0
STAT5 Transcription Factor
0
Stat5a protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101026Subventions
Organisme : European Research Council
ID : 636855
Pays : International
Organisme : Austrian Science Fund FWF
ID : I 4157
Pays : Austria
Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier GmbH.. All rights reserved.
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