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Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity
E. Dalmas, A. Toubal, F. Alzaid, K. Blazek, HL. Eames, K. Lebozec, M. Pini, I. Hainault, E. Montastier, RG. Denis, P. Ancel, A. Lacombe, Y. Ling, O. Allatif, C. Cruciani-Guglielmacci, S. André, N. Viguerie, C. Poitou, V. Stich, A. Torcivia, F....
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 1995-01-01 do 2017-12-31
Medline Complete (EBSCOhost)
od 1998-09-01 do 2015-11-30
Health & Medicine (ProQuest)
od 1995-01-01 do 2017-12-31
PubMed
25939064
DOI
10.1038/nm.3829
Knihovny.cz E-zdroje
- MeSH
- bílá tuková tkáň metabolismus MeSH
- dieta s vysokým obsahem tuků MeSH
- interferonové regulační faktory genetika MeSH
- inzulinová rezistence genetika MeSH
- lidé MeSH
- makrofágy MeSH
- myši MeSH
- obezita farmakoterapie genetika patologie MeSH
- regulace genové exprese MeSH
- transformující růstový faktor beta1 biosyntéza MeSH
- zánět farmakoterapie genetika patologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Accumulation of visceral adipose tissue correlates with elevated inflammation and increased risk of metabolic diseases. However, little is known about the molecular mechanisms that control its pathological expansion. Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype. Here we demonstrate that mice lacking Irf5, when placed on a high-fat diet, show no difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice on the same diet. EpiWAT from Irf5-deficient mice is marked by accumulation of alternatively activated macrophages, higher collagen deposition that restricts adipocyte size, and enhanced insulin sensitivity compared to epiWAT from WT mice. In obese individuals, IRF5 expression is negatively associated with insulin sensitivity and collagen deposition in visceral adipose tissue. Genome-wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth factor β1 (TGFB1) gene itself as a direct target of IRF5-mediated inhibition. This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity, and it suggests that inhibition of IRF5 may promote a healthy metabolic state during this condition.
] Sorbonne Universités Université Pierre et Marie Curie
Institute of Cardiometabolism and Nutrition Paris France
Kennedy Institute Trust of Rheumatology University of Oxford Oxford UK
Citace poskytuje Crossref.org
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- $a Dalmas, Elise $u 1] Sorbonne Universités, Université Pierre et Marie-Curie; INSERM UMR_S 1166-ICAN, Nutriomics, Paris, France. [2] Institute of Cardiometabolism and Nutrition, Paris, France.
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- $a Accumulation of visceral adipose tissue correlates with elevated inflammation and increased risk of metabolic diseases. However, little is known about the molecular mechanisms that control its pathological expansion. Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype. Here we demonstrate that mice lacking Irf5, when placed on a high-fat diet, show no difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice on the same diet. EpiWAT from Irf5-deficient mice is marked by accumulation of alternatively activated macrophages, higher collagen deposition that restricts adipocyte size, and enhanced insulin sensitivity compared to epiWAT from WT mice. In obese individuals, IRF5 expression is negatively associated with insulin sensitivity and collagen deposition in visceral adipose tissue. Genome-wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth factor β1 (TGFB1) gene itself as a direct target of IRF5-mediated inhibition. This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity, and it suggests that inhibition of IRF5 may promote a healthy metabolic state during this condition.
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