Reduced oxidative capacity in macrophages results in systemic insulin resistance
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 rever...
Main Authors: | , , , , , , , , , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Publishing Group
2018-04-01
|
Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-018-03998-z |
id |
doaj-e543088fca854de18576144178eee3f2 |
---|---|
record_format |
Article |
spelling |
doaj-e543088fca854de18576144178eee3f22021-05-11T09:22:08ZengNature Publishing GroupNature Communications2041-17232018-04-019111510.1038/s41467-018-03998-zReduced oxidative capacity in macrophages results in systemic insulin resistanceSaet-Byel Jung0Min Jeong Choi1Dongryeol Ryu2Hyon-Seung Yi3Seong Eun Lee4Joon Young Chang5Hyo Kyun Chung6Yong Kyung Kim7Seul Gi Kang8Ju Hee Lee9Koon Soon Kim10Hyun Jin Kim11Cuk-Seong Kim12Chul-Ho Lee13Robert W. Williams14Hail Kim15Heung Kyu Lee16Johan Auwerx17Minho Shong18Research Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityLaboratory for Integrative and Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de LausanneDepartment of Internal Medicine, Chungnam National University HospitalResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityDepartment of Internal Medicine, Chungnam National University HospitalResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityDepartment of Internal Medicine, Chungnam National University HospitalDepartment of Physiology, Department of Medical Science, School of Medicine, Chungnam National UniversityLaboratory Animal Resource Center, Korea Research Institute of Bioscience and BiotechnologyDepartment of Genetics, Genomics and Informatics, University of Tennessee Health Science CenterGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and TechnologyGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and TechnologyLaboratory for Integrative and Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de LausanneResearch Center for Endocrine and Metabolic Diseases, Department of Medical Science, School of Medicine, Chungnam National UniversityM1-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.https://doi.org/10.1038/s41467-018-03998-z |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Saet-Byel Jung Min Jeong Choi Dongryeol Ryu Hyon-Seung Yi Seong Eun Lee Joon Young Chang Hyo Kyun Chung Yong Kyung Kim Seul Gi Kang Ju Hee Lee Koon Soon Kim Hyun Jin Kim Cuk-Seong Kim Chul-Ho Lee Robert W. Williams Hail Kim Heung Kyu Lee Johan Auwerx Minho Shong |
spellingShingle |
Saet-Byel Jung Min Jeong Choi Dongryeol Ryu Hyon-Seung Yi Seong Eun Lee Joon Young Chang Hyo Kyun Chung Yong Kyung Kim Seul Gi Kang Ju Hee Lee Koon Soon Kim Hyun Jin Kim Cuk-Seong Kim Chul-Ho Lee Robert W. Williams Hail Kim Heung Kyu Lee Johan Auwerx Minho Shong Reduced oxidative capacity in macrophages results in systemic insulin resistance Nature Communications |
author_facet |
Saet-Byel Jung Min Jeong Choi Dongryeol Ryu Hyon-Seung Yi Seong Eun Lee Joon Young Chang Hyo Kyun Chung Yong Kyung Kim Seul Gi Kang Ju Hee Lee Koon Soon Kim Hyun Jin Kim Cuk-Seong Kim Chul-Ho Lee Robert W. Williams Hail Kim Heung Kyu Lee Johan Auwerx Minho Shong |
author_sort |
Saet-Byel Jung |
title |
Reduced oxidative capacity in macrophages results in systemic insulin resistance |
title_short |
Reduced oxidative capacity in macrophages results in systemic insulin resistance |
title_full |
Reduced oxidative capacity in macrophages results in systemic insulin resistance |
title_fullStr |
Reduced oxidative capacity in macrophages results in systemic insulin resistance |
title_full_unstemmed |
Reduced oxidative capacity in macrophages results in systemic insulin resistance |
title_sort |
reduced oxidative capacity in macrophages results in systemic insulin resistance |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2018-04-01 |
description |
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. |
url |
https://doi.org/10.1038/s41467-018-03998-z |
work_keys_str_mv |
AT saetbyeljung reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT minjeongchoi reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT dongryeolryu reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT hyonseungyi reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT seongeunlee reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT joonyoungchang reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT hyokyunchung reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT yongkyungkim reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT seulgikang reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT juheelee reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT koonsoonkim reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT hyunjinkim reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT cukseongkim reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT chulholee reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT robertwwilliams reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT hailkim reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT heungkyulee reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT johanauwerx reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance AT minhoshong reducedoxidativecapacityinmacrophagesresultsinsystemicinsulinresistance |
_version_ |
1721450042142752768 |