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Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness.
Sci. Rep. 6:28080 (2016)
Recently thioredoxin reductase 1 (TrxR1), encoded by Txnrd1, was suggested to modulate glucose and lipid metabolism in mice. Here we discovered that TrxR1 suppresses insulin responsiveness, anabolic metabolism and adipocyte differentiation. Immortalized mouse embryonic fibroblasts (MEFs) lacking Txnrd1 (Txnrd1(-/-)) displayed increased metabolic flux, glycogen storage, lipogenesis and adipogenesis. This phenotype coincided with upregulated PPARγ expression, promotion of mitotic clonal expansion and downregulation of p27 and p53. Enhanced Akt activation also contributed to augmented adipogenesis and insulin sensitivity. Knockdown of TXNRD1 transcripts accelerated adipocyte differentiation also in human primary preadipocytes. Furthermore, TXNRD1 transcript levels in subcutaneous adipose tissue from 56 women were inversely associated with insulin sensitivity in vivo and lipogenesis in their isolated adipocytes. These results suggest that TrxR1 suppresses anabolic metabolism and adipogenesis by inhibition of intracellular signaling pathways downstream of insulin stimulation.
Impact Factor
Scopus SNIP
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Times Cited
Times Cited
Scopus
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Cited By
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5.288
1.589
25
29
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Mitotic Clonal Expansion; Oxygen Species Mediate; Adipose-tissue; Cell-cycle; Adiponectin Production; Binding-protein; Oxidized Ptp1b; Human Obesity; Mice Lacking; Adipogenesis
Language
english
Publication Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
2045-2322
e-ISSN
2045-2322
Journal
Scientific Reports
Quellenangaben
Volume: 6,
Article Number: 28080
Publisher
Nature Publishing Group
Publishing Place
London
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Genetics and Epidemiology
PSP Element(s)
G-500500-004
PubMed ID
27346647
WOS ID
WOS:000378521700001
Scopus ID
84976615559
Erfassungsdatum
2016-06-29