Unique metabolic activation of adipose tissue macrophages in obesity promotes inflammatory responses
Aims/hypothesis Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance,...
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| Vydané v: | Diabetologia Ročník 61; číslo 4; s. 942 - 953 |
|---|---|
| Hlavní autori: | , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.04.2018
Springer Nature B.V |
| Predmet: | |
| ISSN: | 0012-186X, 1432-0428, 1432-0428 |
| On-line prístup: | Získať plný text |
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| Abstract | Aims/hypothesis
Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions.
Methods
F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific
Hif1α
−/−
mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production.
Results
Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14
+
cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity.
Conclusions/interpretation
Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity.
Data availability
Microarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000). |
|---|---|
| AbstractList | Aims/hypothesisRecent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions.MethodsF4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α−/− mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production.ResultsTranscriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14+ cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity.Conclusions/interpretationOur results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity.Data availabilityMicroarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000). Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions.AIMS/HYPOTHESISRecent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions.F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α-/- mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production.METHODSF4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α-/- mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production.Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14+ cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity.RESULTSTranscriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14+ cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity.Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity.CONCLUSIONS/INTERPRETATIONOur results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity.Microarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000).DATA AVAILABILITYMicroarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000). Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions. F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production. Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14 cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity. Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity. Microarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000). Aims/hypothesis: Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions. Methods: F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α−/− mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production. Results: Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14+ cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity. Conclusions/interpretation: Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity. Aims/hypothesis Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions. Methods F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1α −/− mice was used to examine the role of hypoxia-inducible factor-1α (HIF-1α) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production. Results Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14 + cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1α, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity. Conclusions/interpretation Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity. Data availability Microarray data of ATMs isolated from obese or lean mice have been submitted to the Gene Expression Omnibus (accession no. GSE84000). |
| Author | Hooiveld, Guido J. Boutens, Lily Stienstra, Rinke Dhingra, Sourabh Cramer, Robert A. Netea, Mihai G. |
| Author_xml | – sequence: 1 givenname: Lily surname: Boutens fullname: Boutens, Lily organization: Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, Department of Internal Medicine, Radboud University Nijmegen Medical Centre – sequence: 2 givenname: Guido J. surname: Hooiveld fullname: Hooiveld, Guido J. organization: Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University – sequence: 3 givenname: Sourabh surname: Dhingra fullname: Dhingra, Sourabh organization: Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth – sequence: 4 givenname: Robert A. surname: Cramer fullname: Cramer, Robert A. organization: Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth – sequence: 5 givenname: Mihai G. surname: Netea fullname: Netea, Mihai G. organization: Department of Internal Medicine, Radboud University Nijmegen Medical Centre – sequence: 6 givenname: Rinke surname: Stienstra fullname: Stienstra, Rinke email: Rinke.Stienstra@radboudumc.nl organization: Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, Department of Internal Medicine, Radboud University Nijmegen Medical Centre |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29333574$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1530/eje.0.1480535 10.1038/nri2784 10.1038/ni.2419 10.2337/db06-1076 10.2337/db14-0256 10.1016/j.cell.2014.04.016 10.1096/fasebj.6.7.1563593 10.1038/nmicrobiol.2016.246 10.1172/JCI200319246 10.1016/j.immuni.2014.01.006 10.1016/j.cmet.2013.11.001 10.1172/JCI119422 10.1038/nature11862 10.1194/jlr.M064089 10.1074/jbc.M109.018556 10.1074/jbc.M706706200 10.1038/nri978 10.1016/j.cmet.2014.08.010 10.1126/science.1219179 10.1016/j.cmet.2015.07.020 10.1038/nutd.2012.3 10.2337/db16-0012 10.4049/jimmunol.164.12.6166 10.1038/ijo.2010.103 10.1016/j.mito.2013.09.005 10.1172/JCI29881 10.1007/s11626-013-9629-x 10.1016/S0092-8674(03)00154-5 10.1172/JCI84431 10.1038/sj.ijo.0803259 10.1210/en.2014-1689 10.2337/db09-0287 10.1016/j.immuni.2015.02.005 10.1038/nature13490 10.1074/jbc.M110.100263 10.1194/jlr.M500294-JLR200 10.1084/jem.20151570 10.1007/s00125-016-3904-9 10.1172/JCI200319451 10.1126/science.7678183 10.3389/fimmu.2017.00061 |
| ContentType | Journal Article |
| Copyright | The Author(s) 2018 Diabetologia is a copyright of Springer, (2018). All Rights Reserved. Wageningen University & Research |
| Copyright_xml | – notice: The Author(s) 2018 – notice: Diabetologia is a copyright of Springer, (2018). All Rights Reserved. – notice: Wageningen University & Research |
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| DOI | 10.1007/s00125-017-4526-6 |
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| Keywords | Immunometabolism Inflammation Adipose tissue Glycolysis obesity Oxidative phosphorylation Macrophages |
| Language | English |
| License | Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
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| PublicationSubtitle | Clinical, Translational and Experimental Diabetes and Metabolism |
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| References | Stienstra, Dijk, van Beek (CR38) 2014; 63 Maya-Monteiro, Almeida, D’Avila (CR25) 2008; 283 Bruun, Verdich, Toubro, Astrup, Richelsen (CR20) 2003; 148 Baixauli, Acin-Perez, Villarroya-Beltri (CR37) 2015; 22 Xu, Grijalva, Skowronski, van Eijk, Serlie, Ferrante (CR10) 2013; 18 Wentworth, Naselli, Brown (CR3) 2010; 59 Bigornia, Farb, Mott (CR1) 2012; 2 Gautier, Shay, Miller (CR7) 2012; 13 Schottl, Kappler, Braun, Fromme, Klingenspor (CR29) 2015; 156 Lachmandas, Boutens (CR36) 2016; 2 Cramer, Yamanishi, Clausen (CR15) 2003; 112 Okabe, Medzhitov (CR16) 2014; 157 Xue, Schmidt, Sander (CR8) 2014; 40 Lumeng, Bodzin, Saltiel (CR6) 2007; 117 Lumeng, Deyoung, Bodzin, Saltiel (CR2) 2007; 56 Corcoran, O’Neill (CR14) 2016; 126 Zeyda, Gollinger, Kriehuber, Kiefer, Neuhofer, Stulnig (CR31) 2010; 34 Weisberg, McCann, Desai, Rosenbaum, Leibel, Ferrante (CR35) 2003; 112 Hotamisligil, Shargill, Spiegelman (CR33) 1993; 259 Cinti, Mitchell, Barbatelli (CR40) 2005; 46 Xu, Barnes, Yang (CR34) 2003; 112 Haka, Barbosa-Lorenzi, Lee (CR39) 2016; 57 Langston, Shibata, Horng (CR13) 2017; 8 O’Neill, Pearce (CR12) 2016; 213 Kim, Park, Kawada (CR21) 2006; 30 O'Neill, Hardie (CR27) 2013; 493 Jha, Huang, Sergushichev (CR11) 2015; 42 Kratz, Coats, Hisert (CR9) 2014; 20 Geissmann, Gordon, Hume, Mowat, Randolph (CR17) 2010; 10 DiGirolamo, Newby, Lovejoy (CR23) 1992; 6 Colegio, Chu, Szabo (CR26) 2014; 513 Neels, Badeanlou, Hester, Samad (CR19) 2009; 284 Lonnqvist, Nordfors, Jansson, Thorne, Schalling, Arner (CR22) 1997; 99 Li, Lu, Nguyen (CR32) 2010; 285 Nickens, Wikstrom, Shirihai, Patierno, Ceryak (CR28) 2013; 13 Acedo, Gambero, Cunha, Lorand-Metze, Gambero (CR24) 2013; 49 Takikawa, Mahmood, Nawaz (CR41) 2016; 65 Gordon (CR4) 2003; 3 Schulz, Gomez Perdiguero, Chorro (CR18) 2012; 336 Mills, Kincaid, Alt, Heilman, Hill (CR5) 2000; 164 Boutens, Stienstra (CR30) 2016; 59 AS Haka (4526_CR39) 2016; 57 EL Gautier (4526_CR7) 2012; 13 JG Neels (4526_CR19) 2009; 284 F Geissmann (4526_CR17) 2010; 10 CS Kim (4526_CR21) 2006; 30 CM Maya-Monteiro (4526_CR25) 2008; 283 SJ Bigornia (4526_CR1) 2012; 2 PK Langston (4526_CR13) 2017; 8 M DiGirolamo (4526_CR23) 1992; 6 C Schulz (4526_CR18) 2012; 336 L Boutens (4526_CR30) 2016; 59 GS Hotamisligil (4526_CR33) 1993; 259 A Takikawa (4526_CR41) 2016; 65 SC Acedo (4526_CR24) 2013; 49 T Schottl (4526_CR29) 2015; 156 SE Corcoran (4526_CR14) 2016; 126 AK Jha (4526_CR11) 2015; 42 KP Nickens (4526_CR28) 2013; 13 F Lonnqvist (4526_CR22) 1997; 99 S Cinti (4526_CR40) 2005; 46 T Cramer (4526_CR15) 2003; 112 Y Okabe (4526_CR16) 2014; 157 CD Mills (4526_CR5) 2000; 164 LA O’Neill (4526_CR12) 2016; 213 F Baixauli (4526_CR37) 2015; 22 P Li (4526_CR32) 2010; 285 J Xue (4526_CR8) 2014; 40 CN Lumeng (4526_CR2) 2007; 56 H Xu (4526_CR34) 2003; 112 E Lachmandas (4526_CR36) 2016; 2 X Xu (4526_CR10) 2013; 18 JM Bruun (4526_CR20) 2003; 148 LA O'Neill (4526_CR27) 2013; 493 JM Wentworth (4526_CR3) 2010; 59 M Kratz (4526_CR9) 2014; 20 SP Weisberg (4526_CR35) 2003; 112 M Zeyda (4526_CR31) 2010; 34 CN Lumeng (4526_CR6) 2007; 117 S Gordon (4526_CR4) 2003; 3 OR Colegio (4526_CR26) 2014; 513 R Stienstra (4526_CR38) 2014; 63 |
| References_xml | – volume: 148 start-page: 535 year: 2003 end-page: 542 ident: CR20 article-title: Association between measures of insulin sensitivity and circulating levels of interleukin-8, interleukin-6 and tumor necrosis factor-alpha. Effect of weight loss in obese men publication-title: Eur J Endocrinol doi: 10.1530/eje.0.1480535 – volume: 10 start-page: 453 year: 2010 end-page: 460 ident: CR17 article-title: Unravelling mononuclear phagocyte heterogeneity publication-title: Nat Rev Immunol doi: 10.1038/nri2784 – volume: 13 start-page: 1118 year: 2012 end-page: 1128 ident: CR7 article-title: Gene-expression profiles and transcriptional regulatory pathways that underlie the identity and diversity of mouse tissue macrophages publication-title: Nat Immunol doi: 10.1038/ni.2419 – volume: 56 start-page: 16 year: 2007 end-page: 23 ident: CR2 article-title: Increased inflammatory properties of adipose tissue macrophages recruited during diet-induced obesity publication-title: Diabetes doi: 10.2337/db06-1076 – volume: 63 start-page: 4143 year: 2014 end-page: 4153 ident: CR38 article-title: Mannose-binding lectin is required for the effective clearance of apoptotic cells by adipose tissue macrophages during obesity publication-title: Diabetes doi: 10.2337/db14-0256 – volume: 157 start-page: 832 year: 2014 end-page: 844 ident: CR16 article-title: Tissue-specific signals control reversible program of localization and functional polarization of macrophages publication-title: Cell doi: 10.1016/j.cell.2014.04.016 – volume: 6 start-page: 2405 year: 1992 end-page: 2412 ident: CR23 article-title: Lactate production in adipose tissue: a regulated function with extra-adipose implications publication-title: FASEB J doi: 10.1096/fasebj.6.7.1563593 – volume: 2 start-page: 16246 year: 2016 ident: CR36 article-title: Microbial stimulation of different toll-like receptor signalling pathways induces diverse metabolic programmes in human monocytes publication-title: Nat Microbiol doi: 10.1038/nmicrobiol.2016.246 – volume: 112 start-page: 1796 year: 2003 end-page: 1808 ident: CR35 article-title: Obesity is associated with macrophage accumulation in adipose tissue publication-title: J Clin Invest doi: 10.1172/JCI200319246 – volume: 40 start-page: 274 year: 2014 end-page: 288 ident: CR8 article-title: Transcriptome-based network analysis reveals a spectrum model of human macrophage activation publication-title: Immunity doi: 10.1016/j.immuni.2014.01.006 – volume: 18 start-page: 816 year: 2013 end-page: 830 ident: CR10 article-title: Obesity activates a program of lysosomal-dependent lipid metabolism in adipose tissue macrophages independently of classic activation publication-title: Cell Metab doi: 10.1016/j.cmet.2013.11.001 – volume: 99 start-page: 2398 year: 1997 end-page: 2404 ident: CR22 article-title: Leptin secretion from adipose tissue in women. Relationship to plasma levels and gene expression publication-title: J Clin Invest doi: 10.1172/JCI119422 – volume: 493 start-page: 346 year: 2013 end-page: 355 ident: CR27 article-title: Metabolism of inflammation limited by AMPK and pseudo-starvation publication-title: Nature doi: 10.1038/nature11862 – volume: 57 start-page: 980 year: 2016 end-page: 992 ident: CR39 article-title: Exocytosis of macrophage lysosomes leads to digestion of apoptotic adipocytes and foam cell formation publication-title: J Lipid Res doi: 10.1194/jlr.M064089 – volume: 284 start-page: 20692 year: 2009 end-page: 20698 ident: CR19 article-title: Keratinocyte-derived chemokine in obesity: expression, regulation, and role in adipose macrophage infiltration and glucose homeostasis publication-title: J Biol Chem doi: 10.1074/jbc.M109.018556 – volume: 283 start-page: 2203 year: 2008 end-page: 2210 ident: CR25 article-title: Leptin induces macrophage lipid body formation by a phosphatidylinositol 3-kinase- and mammalian target of rapamycin-dependent mechanism publication-title: J Biol Chem doi: 10.1074/jbc.M706706200 – volume: 3 start-page: 23 year: 2003 end-page: 35 ident: CR4 article-title: Alternative activation of macrophages publication-title: Nat Rev Immunol doi: 10.1038/nri978 – volume: 20 start-page: 614 year: 2014 end-page: 625 ident: CR9 article-title: Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages publication-title: Cell Metab doi: 10.1016/j.cmet.2014.08.010 – volume: 336 start-page: 86 year: 2012 end-page: 90 ident: CR18 article-title: A lineage of myeloid cells independent of Myb and hematopoietic stem cells publication-title: Science doi: 10.1126/science.1219179 – volume: 22 start-page: 485 year: 2015 end-page: 498 ident: CR37 article-title: Mitochondrial respiration controls lysosomal function during inflammatory T cell responses publication-title: Cell Metab doi: 10.1016/j.cmet.2015.07.020 – volume: 2 start-page: e30 year: 2012 ident: CR1 article-title: Relation of depot-specific adipose inflammation to insulin resistance in human obesity publication-title: Nutr Diabetes doi: 10.1038/nutd.2012.3 – volume: 65 start-page: 3649 year: 2016 end-page: 3659 ident: CR41 article-title: HIF-1α in myeloid cells promotes adipose tissue remodeling toward insulin resistance publication-title: Diabetes doi: 10.2337/db16-0012 – volume: 164 start-page: 6166 year: 2000 end-page: 6173 ident: CR5 article-title: M-1/M-2 macrophages and the Th1/Th2 paradigm publication-title: J Immunol doi: 10.4049/jimmunol.164.12.6166 – volume: 34 start-page: 1684 year: 2010 end-page: 1694 ident: CR31 article-title: Newly identified adipose tissue macrophage populations in obesity with distinct chemokine and chemokine receptor expression publication-title: Int J Obes doi: 10.1038/ijo.2010.103 – volume: 13 start-page: 662 year: 2013 end-page: 667 ident: CR28 article-title: A bioenergetic profile of non-transformed fibroblasts uncovers a link between death-resistance and enhanced spare respiratory capacity publication-title: Mitochondrion doi: 10.1016/j.mito.2013.09.005 – volume: 117 start-page: 175 year: 2007 end-page: 184 ident: CR6 article-title: Obesity induces a phenotypic switch in adipose tissue macrophage polarization publication-title: J Clin Invest doi: 10.1172/JCI29881 – volume: 49 start-page: 473 year: 2013 end-page: 478 ident: CR24 article-title: Participation of leptin in the determination of the macrophage phenotype: an additional role in adipocyte and macrophage crosstalk publication-title: In Vitro Cell Dev Biol Anim doi: 10.1007/s11626-013-9629-x – volume: 112 start-page: 645 year: 2003 end-page: 657 ident: CR15 article-title: HIF-1α is essential for myeloid cell-mediated inflammation publication-title: Cell doi: 10.1016/S0092-8674(03)00154-5 – volume: 126 start-page: 3699 year: 2016 end-page: 3707 ident: CR14 article-title: HIF1α and metabolic reprogramming in inflammation publication-title: J Clin Invest doi: 10.1172/JCI84431 – volume: 30 start-page: 1347 year: 2006 end-page: 1355 ident: CR21 article-title: Circulating levels of MCP-1 and IL-8 are elevated in human obese subjects and associated with obesity-related parameters publication-title: Int J Obes doi: 10.1038/sj.ijo.0803259 – volume: 156 start-page: 923 year: 2015 end-page: 933 ident: CR29 article-title: Limited mitochondrial capacity of visceral versus subcutaneous white adipocytes in male C57BL/6N mice publication-title: Endocrinology doi: 10.1210/en.2014-1689 – volume: 59 start-page: 1648 year: 2010 end-page: 1656 ident: CR3 article-title: Pro-inflammatory CD11c CD206 adipose tissue macrophages are associated with insulin resistance in human obesity publication-title: Diabetes doi: 10.2337/db09-0287 – volume: 42 start-page: 419 year: 2015 end-page: 430 ident: CR11 article-title: Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization publication-title: Immunity doi: 10.1016/j.immuni.2015.02.005 – volume: 513 start-page: 559 year: 2014 end-page: 563 ident: CR26 article-title: Functional polarization of tumour-associated macrophages by tumour-derived lactic acid publication-title: Nature doi: 10.1038/nature13490 – volume: 285 start-page: 15333 year: 2010 end-page: 15345 ident: CR32 article-title: Functional heterogeneity of CD11c-positive adipose tissue macrophages in diet-induced obese mice publication-title: J Biol Chem doi: 10.1074/jbc.M110.100263 – volume: 46 start-page: 2347 year: 2005 end-page: 2355 ident: CR40 article-title: Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans publication-title: J Lipid Res doi: 10.1194/jlr.M500294-JLR200 – volume: 213 start-page: 15 year: 2016 end-page: 23 ident: CR12 article-title: Immunometabolism governs dendritic cell and macrophage function publication-title: J Exp Med doi: 10.1084/jem.20151570 – volume: 59 start-page: 879 year: 2016 end-page: 894 ident: CR30 article-title: Adipose tissue macrophages: going off track during obesity publication-title: Diabetologia doi: 10.1007/s00125-016-3904-9 – volume: 112 start-page: 1821 year: 2003 end-page: 1830 ident: CR34 article-title: Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance publication-title: J Clin Invest doi: 10.1172/JCI200319451 – volume: 259 start-page: 87 year: 1993 end-page: 91 ident: CR33 article-title: Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance publication-title: Science doi: 10.1126/science.7678183 – volume: 8 start-page: 61 year: 2017 ident: CR13 article-title: Metabolism supports macrophage activation publication-title: Front Immunol doi: 10.3389/fimmu.2017.00061 – volume: 22 start-page: 485 year: 2015 ident: 4526_CR37 publication-title: Cell Metab doi: 10.1016/j.cmet.2015.07.020 – volume: 63 start-page: 4143 year: 2014 ident: 4526_CR38 publication-title: Diabetes doi: 10.2337/db14-0256 – volume: 40 start-page: 274 year: 2014 ident: 4526_CR8 publication-title: Immunity doi: 10.1016/j.immuni.2014.01.006 – volume: 49 start-page: 473 year: 2013 ident: 4526_CR24 publication-title: In Vitro Cell Dev Biol Anim doi: 10.1007/s11626-013-9629-x – volume: 336 start-page: 86 year: 2012 ident: 4526_CR18 publication-title: Science doi: 10.1126/science.1219179 – volume: 59 start-page: 879 year: 2016 ident: 4526_CR30 publication-title: Diabetologia doi: 10.1007/s00125-016-3904-9 – volume: 112 start-page: 1796 year: 2003 ident: 4526_CR35 publication-title: J Clin Invest doi: 10.1172/JCI200319246 – volume: 99 start-page: 2398 year: 1997 ident: 4526_CR22 publication-title: J Clin Invest doi: 10.1172/JCI119422 – volume: 59 start-page: 1648 year: 2010 ident: 4526_CR3 publication-title: Diabetes doi: 10.2337/db09-0287 – volume: 126 start-page: 3699 year: 2016 ident: 4526_CR14 publication-title: J Clin Invest doi: 10.1172/JCI84431 – volume: 513 start-page: 559 year: 2014 ident: 4526_CR26 publication-title: Nature doi: 10.1038/nature13490 – volume: 2 start-page: 16246 year: 2016 ident: 4526_CR36 publication-title: Nat Microbiol doi: 10.1038/nmicrobiol.2016.246 – volume: 117 start-page: 175 year: 2007 ident: 4526_CR6 publication-title: J Clin Invest doi: 10.1172/JCI29881 – volume: 157 start-page: 832 year: 2014 ident: 4526_CR16 publication-title: Cell doi: 10.1016/j.cell.2014.04.016 – volume: 283 start-page: 2203 year: 2008 ident: 4526_CR25 publication-title: J Biol Chem doi: 10.1074/jbc.M706706200 – volume: 112 start-page: 645 year: 2003 ident: 4526_CR15 publication-title: Cell doi: 10.1016/S0092-8674(03)00154-5 – volume: 65 start-page: 3649 year: 2016 ident: 4526_CR41 publication-title: Diabetes doi: 10.2337/db16-0012 – volume: 56 start-page: 16 year: 2007 ident: 4526_CR2 publication-title: Diabetes doi: 10.2337/db06-1076 – volume: 42 start-page: 419 year: 2015 ident: 4526_CR11 publication-title: Immunity doi: 10.1016/j.immuni.2015.02.005 – volume: 18 start-page: 816 year: 2013 ident: 4526_CR10 publication-title: Cell Metab doi: 10.1016/j.cmet.2013.11.001 – volume: 20 start-page: 614 year: 2014 ident: 4526_CR9 publication-title: Cell Metab doi: 10.1016/j.cmet.2014.08.010 – volume: 493 start-page: 346 year: 2013 ident: 4526_CR27 publication-title: Nature doi: 10.1038/nature11862 – volume: 57 start-page: 980 year: 2016 ident: 4526_CR39 publication-title: J Lipid Res doi: 10.1194/jlr.M064089 – volume: 164 start-page: 6166 year: 2000 ident: 4526_CR5 publication-title: J Immunol doi: 10.4049/jimmunol.164.12.6166 – volume: 10 start-page: 453 year: 2010 ident: 4526_CR17 publication-title: Nat Rev Immunol doi: 10.1038/nri2784 – volume: 112 start-page: 1821 year: 2003 ident: 4526_CR34 publication-title: J Clin Invest doi: 10.1172/JCI200319451 – volume: 46 start-page: 2347 year: 2005 ident: 4526_CR40 publication-title: J Lipid Res doi: 10.1194/jlr.M500294-JLR200 – volume: 2 start-page: e30 year: 2012 ident: 4526_CR1 publication-title: Nutr Diabetes doi: 10.1038/nutd.2012.3 – volume: 34 start-page: 1684 year: 2010 ident: 4526_CR31 publication-title: Int J Obes doi: 10.1038/ijo.2010.103 – volume: 285 start-page: 15333 year: 2010 ident: 4526_CR32 publication-title: J Biol Chem doi: 10.1074/jbc.M110.100263 – volume: 13 start-page: 1118 year: 2012 ident: 4526_CR7 publication-title: Nat Immunol doi: 10.1038/ni.2419 – volume: 8 start-page: 61 year: 2017 ident: 4526_CR13 publication-title: Front Immunol doi: 10.3389/fimmu.2017.00061 – volume: 13 start-page: 662 year: 2013 ident: 4526_CR28 publication-title: Mitochondrion doi: 10.1016/j.mito.2013.09.005 – volume: 284 start-page: 20692 year: 2009 ident: 4526_CR19 publication-title: J Biol Chem doi: 10.1074/jbc.M109.018556 – volume: 213 start-page: 15 year: 2016 ident: 4526_CR12 publication-title: J Exp Med doi: 10.1084/jem.20151570 – volume: 259 start-page: 87 year: 1993 ident: 4526_CR33 publication-title: Science doi: 10.1126/science.7678183 – volume: 156 start-page: 923 year: 2015 ident: 4526_CR29 publication-title: Endocrinology doi: 10.1210/en.2014-1689 – volume: 148 start-page: 535 year: 2003 ident: 4526_CR20 publication-title: Eur J Endocrinol doi: 10.1530/eje.0.1480535 – volume: 30 start-page: 1347 year: 2006 ident: 4526_CR21 publication-title: Int J Obes doi: 10.1038/sj.ijo.0803259 – volume: 6 start-page: 2405 year: 1992 ident: 4526_CR23 publication-title: FASEB J doi: 10.1096/fasebj.6.7.1563593 – volume: 3 start-page: 23 year: 2003 ident: 4526_CR4 publication-title: Nat Rev Immunol doi: 10.1038/nri978 |
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Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory... Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate... Aims/hypothesisRecent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory... Aims/hypothesis: Recent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory... |
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| SubjectTerms | Activation, Metabolic Adipocytes - metabolism Adipose tissue Adipose Tissue - cytology Animals Bone marrow CD14 antigen Cell activation Chair Nutrition Metabolism and Genomics Cytokines Cytokines - metabolism Diabetes mellitus DNA microarrays Energy metabolism Enzyme-linked immunosorbent assay Explants Gene expression Gene Expression Profiling Gene Expression Regulation Glycolysis HNE Nutrition, Metabolism and Genomics HNE Voeding, Metabolisme en Genomics Human Physiology Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-inducible factor 1a Inflammation Insulin Insulin Resistance Internal Medicine Intracellular Lactic acid Leptin Macrophages Macrophages - metabolism Male Medicine Medicine & Public Health Metabolic activation Metabolic Diseases Metabolic rate Metabolism Mice Mice, Inbred C57BL Mice, Knockout Myeloid Cells - cytology Nutrition, Metabolism and Genomics Obesity Obesity - metabolism Oxidation Oxidative phosphorylation Oxygen - chemistry Peritoneum Phenotype VLAG Voeding, Metabolisme en Genomica |
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| Title | Unique metabolic activation of adipose tissue macrophages in obesity promotes inflammatory responses |
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