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...

Full description

Bibliographic Details
Main Authors: 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
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