Reduced oxidative capacity in macrophages results in systemic insulin resistance
Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPho...
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| Published in | Nature communications Vol. 9; no. 1; pp. 1551 - 15 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
19.04.2018
Nature Publishing Group Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-1723 2041-1723 |
| DOI | 10.1038/s41467-018-03998-z |
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| Abstract | Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (
Crif1
), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in
ob/ob
mice and HFD-fed mice with myeloid-specific deletion of
Crif1
. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages.
M1-like polarization of macrophages is thought to control adipose inflammation and associated insulin resistance and metabolic syndrome. Here the authors show that macrophage-specific deletion of the OxPhos-related gene
Crif1
results in an M1-like phenotype in mice, and that the effects can be reversed by recombinant GDF15. |
|---|---|
| AbstractList | Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages. Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 ( Crif1 ), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1 . Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages. Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 ( Crif1 ), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1 . Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages. M1-like polarization of macrophages is thought to control adipose inflammation and associated insulin resistance and metabolic syndrome. Here the authors show that macrophage-specific deletion of the OxPhos-related gene Crif1 results in an M1-like phenotype in mice, and that the effects can be reversed by recombinant GDF15. M1-like polarization of macrophages is thought to control adipose inflammation and associated insulin resistance and metabolic syndrome. Here the authors show that macrophage-specific deletion of the OxPhos-related gene Crif1 results in an M1-like phenotype in mice, and that the effects can be reversed by recombinant GDF15. Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages.Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages. Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages. M1-like polarization of macrophages is thought to control adipose inflammation and associated insulin resistance and metabolic syndrome. Here the authors show that macrophage-specific deletion of the OxPhos-related gene Crif1 results in an M1-like phenotype in mice, and that the effects can be reversed by recombinant GDF15. |
| ArticleNumber | 1551 |
| Author | Chung, Hyo Kyun Williams, Robert W. Lee, Heung Kyu Kim, Hyun Jin Jung, Saet-Byel Kim, Yong Kyung Choi, Min Jeong Shong, Minho Chang, Joon Young Auwerx, Johan Lee, Chul-Ho Kim, Koon Soon Kim, Cuk-Seong Ryu, Dongryeol Yi, Hyon-Seung Lee, Seong Eun Lee, Ju Hee Kim, Hail Kang, Seul Gi |
| Author_xml | – sequence: 1 givenname: Saet-Byel surname: Jung fullname: Jung, Saet-Byel organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 2 givenname: Min Jeong surname: Choi fullname: Choi, Min Jeong organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 3 givenname: Dongryeol surname: Ryu fullname: Ryu, Dongryeol organization: Laboratory for Integrative and Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de Lausanne, Laboratory of Molecular and Integrative Biology, Department of Korean Medical Science, School of Korean Medicine, Pusan National University – sequence: 4 givenname: Hyon-Seung surname: Yi fullname: Yi, Hyon-Seung organization: Department of Internal Medicine, Chungnam National University Hospital – sequence: 5 givenname: Seong Eun surname: Lee fullname: Lee, Seong Eun organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 6 givenname: Joon Young surname: Chang fullname: Chang, Joon Young organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 7 givenname: Hyo Kyun surname: Chung fullname: Chung, Hyo Kyun organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 8 givenname: Yong Kyung surname: Kim fullname: Kim, Yong Kyung organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 9 givenname: Seul Gi surname: Kang fullname: Kang, Seul Gi organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 10 givenname: Ju Hee surname: Lee fullname: Lee, Ju Hee organization: Department of Internal Medicine, Chungnam National University Hospital – sequence: 11 givenname: Koon Soon surname: Kim fullname: Kim, Koon Soon organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University, Department of Internal Medicine, Chungnam National University Hospital – sequence: 12 givenname: Hyun Jin surname: Kim fullname: Kim, Hyun Jin organization: Department of Internal Medicine, Chungnam National University Hospital – sequence: 13 givenname: Cuk-Seong surname: Kim fullname: Kim, Cuk-Seong organization: Department of Physiology, Department of Medical Science, School of Medicine, Chungnam National University – sequence: 14 givenname: Chul-Ho surname: Lee fullname: Lee, Chul-Ho organization: Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology – sequence: 15 givenname: Robert W. surname: Williams fullname: Williams, Robert W. organization: Department of Genetics, Genomics and Informatics, University of Tennessee Health Science Center – sequence: 16 givenname: Hail surname: Kim fullname: Kim, Hail organization: Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology – sequence: 17 givenname: Heung Kyu orcidid: 0000-0002-3977-1510 surname: Lee fullname: Lee, Heung Kyu organization: Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology – sequence: 18 givenname: Johan surname: Auwerx fullname: Auwerx, Johan organization: Laboratory for Integrative and Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de Lausanne – sequence: 19 givenname: Minho surname: Shong fullname: Shong, Minho email: minhos@cnu.ac.kr organization: Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National University, Department of Internal Medicine, Chungnam National University Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29674655$$D View this record in MEDLINE/PubMed |
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| Snippet | Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function... M1-like polarization of macrophages is thought to control adipose inflammation and associated insulin resistance and metabolic syndrome. Here the authors show... |
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| Title | Reduced oxidative capacity in macrophages results in systemic insulin resistance |
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