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Differential lipid ...
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Prieur, XavierDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom; Institut du Thorax, Institut National de la Santé et de la Recherche Médicale U915, Nantes, France
(author)
Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice
- Article/chapterEnglish2011
Publisher, publication year, extent ...
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2011-02-21
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American Diabetes Association,2011
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LIBRIS-ID:oai:DiVA.org:oru-63642
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-63642URI
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https://doi.org/10.2337/db10-0705DOI
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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Funding agencieas:MRC CORD MRC BHF Spanish Ministry of Science and Innovation SAF2009-07466 BIO BIO2008-04212 Marato TV3 Pro-CNIC Foundation Fundacion IMABIS
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OBJECTIVE: Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response.RESEARCH DESIGN AND METHODS: We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment.RESULTS: We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell-like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization.CONCLUSIONS: Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization.
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Mok, Crystal Y. L.Department of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
(author)
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Velagapudi, Vidya RTechnical Research Centre of Finland (VTT), Espoo, Finland
(author)
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Núñez, VanessaDepartment of Regenerative Cardiology, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
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Fuentes, LucíaDepartment of Regenerative Cardiology, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
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Montaner, DavidDepartment of Bioinformatics and Genomics, Functional Genomics Node (INB) at CIPF, Centro de Investigación Príncipe Felipe (CIFP), Valencia, Spain
(author)
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Ishikawa, KoDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
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Camacho, AlbertoDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
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Barbarroja, NuriaDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
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O'Rahilly, StephenDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
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Sethi, Jaswinder KDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
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Dopazo, JoaquinDepartment of Regenerative Cardiology, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
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Oresic, Matej,1967-Örebro universitet,Institutionen för medicinska vetenskaper,Technical Research Centre of Finland (VTT), Espoo, Finland(Swepub:oru)moc
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Ricote, MercedesDepartment of Regenerative Cardiology, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
(author)
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Vidal-Puig, AntonioDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
(author)
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Department of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom; Institut du Thorax, Institut National de la Santé et de la Recherche Médicale U915, Nantes, FranceDepartment of Clinical Biochemistry, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom
(creator_code:org_t)
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In:Diabetes: American Diabetes Association60:3, s. 797-8090012-17971939-327X
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