Adipocyte STAT5 deficiency does not affect blood glucose homeostasis in obese mice.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2021
Historique:
received: 07 07 2021
accepted: 10 11 2021
entrez: 24 11 2021
pubmed: 25 11 2021
medline: 6 1 2022
Statut: epublish

Résumé

The aim of this study was to investigate whether the lack of signal transducer and activator of transcription 5 (STAT5) in mature adipocytes of obese mice (Stat5Adipoq mice) improves glucose and lipid metabolism as previously observed in lean mice. Male Stat5Adipoq mice and their wild type (WT) littermates were fed high-fat diet (HFD). Effects of adipocyte STAT5 deficiency on adiposity as well as on glucose and lipid metabolism were determined under ad libitum feeding and after weight loss induced by calorie restriction. Compared to WT mice, obese Stat5Adipoq mice showed modestly accelerated weight gain and blunted depletion of fat stores under calorie restriction (reduction in % body fat after 3 weeks: WT, -9.3±1.1, vs Stat5Adipoq, -5.9±0.8, p = 0.04). No differences were observed between Stat5Adipoq and WT mice with regard to parameters of glucose and lipid metabolism including basal glycaemia, glucose tolerance, and plasma triglycerides. In conclusion, STAT5 deficiency in the adipocyte of HFD-fed obese mice was associated with increased fat accumulation. In contrast to previous findings in lean mice, however, lipid accumulation was not associated with any improvement in glucose and lipid metabolism. Our results do not support adipocyte STAT5 as a promising target for the treatment of obesity-associated metabolic derangements.

Identifiants

pubmed: 34818373
doi: 10.1371/journal.pone.0260501
pii: PONE-D-21-21403
pmc: PMC8612524
doi:

Substances chimiques

Blood Glucose 0
STAT5 Transcription Factor 0
Stat5a protein, mouse 0
Stat5b protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0260501

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

Références

J Mol Endocrinol. 2020 Jan;64(1):13-27
pubmed: 31756168
J Exp Med. 2009 Apr 13;206(4):819-31
pubmed: 19332876
Cell Signal. 2015 Dec;27(12):2434-43
pubmed: 26388045
Hepatology. 2007 Aug;46(2):504-13
pubmed: 17640041
Nat Rev Endocrinol. 2020 Mar;16(3):135-146
pubmed: 31780780
Cell. 2012 Mar 2;148(5):852-71
pubmed: 22385956
Endocrinology. 2006 Jun;147(6):2754-63
pubmed: 16513828
Endocrinology. 2019 Jan 1;160(1):68-80
pubmed: 30462209
Biochem Biophys Res Commun. 1999 Aug 19;262(1):216-22
pubmed: 10448095
Mol Metab. 2020 Oct;40:101026
pubmed: 32473405
J Clin Endocrinol Metab. 2001 Aug;86(8):3845-52
pubmed: 11502822
Diabetologia. 2017 Feb;60(2):296-305
pubmed: 27858140
Growth Horm IGF Res. 2018 Oct - Dec;42-43:40-51
pubmed: 30193158
Diabetes. 2013 Mar;62(3):864-74
pubmed: 23321074
J Biol Chem. 1957 May;226(1):497-509
pubmed: 13428781
Diabetes. 2018 Feb;67(2):208-221
pubmed: 29203511
Endocrinology. 2015 Oct;156(10):3610-24
pubmed: 26196542
Metabolism. 1997 Aug;46(8):935-42
pubmed: 9258278
Nat Rev Mol Cell Biol. 2016 Nov;17(11):691-702
pubmed: 27552974
Diabetologia. 2004 Jul;47(7):1306-1313
pubmed: 15232684
Cell Cycle. 2020 Apr;19(8):895-905
pubmed: 32207362
J Clin Invest. 2019 Oct 1;129(10):4022-4031
pubmed: 31573549
Physiol Rep. 2020 Feb;8(3):e14373
pubmed: 32073221
Diabetologia. 2013 May;56(5):1129-39
pubmed: 23423668
Lancet. 2010 Jun 26;375(9733):2267-77
pubmed: 20609972
Nat Rev Endocrinol. 2013 Jun;9(6):346-56
pubmed: 23568441

Auteurs

Marianna Beghini (M)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Theresia Wagner (T)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Andreea Corina Luca (AC)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Matthäus Metz (M)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Doris Kaltenecker (D)

Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.

Katrin Spirk (K)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.

Martina Theresa Hackl (MT)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Johannes Haybaeck (J)

Institute of Pathology, Neuropathology and Molecular Pathology, Medical University of Innsbruck, Innsbruck, Austria.
Diagnostic & Research Center for Molecular Biomedicine, Institute of Pathology, Medical University of Graz, Graz, Austria.

Richard Moriggl (R)

Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.

Alexandra Kautzky-Willer (A)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Thomas Scherer (T)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Clemens Fürnsinn (C)

Division of Endocrinology & Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

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Classifications MeSH