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...

Full description

Saved in:
Bibliographic Details
Published inNature communications Vol. 9; no. 1; pp. 1551 - 15
Main Authors Jung, Saet-Byel, Choi, Min Jeong, Ryu, Dongryeol, Yi, Hyon-Seung, Lee, Seong Eun, Chang, Joon Young, Chung, Hyo Kyun, Kim, Yong Kyung, Kang, Seul Gi, Lee, Ju Hee, Kim, Koon Soon, Kim, Hyun Jin, Kim, Cuk-Seong, Lee, Chul-Ho, Williams, Robert W., Kim, Hail, Lee, Heung Kyu, Auwerx, Johan, Shong, Minho
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 19.04.2018
Nature Publishing Group
Nature Portfolio
Subjects
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-018-03998-z

Cover

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
BookMark eNqNUk1v1DAQtVARLaV_gAOKxIVLwI6_L0ioglKpEgi4W64z2XqV2MFOWra_vt5mKW0PFb7YmnnveebNvER7IQZA6DXB7wmm6kNmhAlZY6JqTLVW9fUzdNBgRmoiG7p3772PjnJe43KoJoqxF2i_0UIywfkB-v4D2tlBW8U_vrWTv4TK2dE6P20qH6rBuhTHC7uCXCXIcz_lbThv8gSDd-VdYiVQcj5PNjh4hZ53ts9wtLsP0c8vn38df63Pvp2cHn86q53AYqo7xbRQ1MlOnDsuXUsJ44pi4ZSkEqjsWmG56rDllDWCYk4obTXlsnHA6SE6XVTbaNdmTH6waWOi9eY2ENPK2DR514MBzihWqnNWcdYCUVwKwhiRCgBo1xQtumjNYbSbK9v3d4IEm63ZZjHbFLPNrdnmurA-LqxxPh-gdRCmZPsHpTzMBH9hVvHScI2V1LoIvNsJpPh7hjyZwWcHfW8DxDmbBjdKC8IVLtC3j6DrOKdQ7N2iJJcYa1ZQb-5XdFfK32EXQLMAykxzTtD9X5_qEansRlmUuO3K909Td8bm8k9YQfpX9hOsG29I3z0
CitedBy_id crossref_primary_10_1016_j_celrep_2023_112424
crossref_primary_10_1371_journal_ppat_1009198
crossref_primary_10_4110_in_2025_25_e9
crossref_primary_10_1186_s13046_020_01595_x
crossref_primary_10_3390_ijms22062854
crossref_primary_10_1002_adhm_202400012
crossref_primary_10_3389_fendo_2018_00485
crossref_primary_10_1016_j_celrep_2020_01_046
crossref_primary_10_1038_s41467_020_20315_9
crossref_primary_10_3389_fphar_2022_887263
crossref_primary_10_20945_2359_4292_2023_0416
crossref_primary_10_1007_s12634_024_2940_6
crossref_primary_10_1016_j_jbc_2023_105566
crossref_primary_10_1016_j_jcmgh_2023_07_009
crossref_primary_10_1016_j_cbpc_2018_08_010
crossref_primary_10_1016_j_bbagen_2020_129834
crossref_primary_10_1016_j_bcp_2022_115337
crossref_primary_10_1016_j_isci_2021_102181
crossref_primary_10_3389_fimmu_2022_823842
crossref_primary_10_1002_biof_1871
crossref_primary_10_1016_j_isci_2023_107376
crossref_primary_10_3389_fimmu_2021_760577
crossref_primary_10_1016_j_jshs_2019_12_003
crossref_primary_10_3390_cells11071249
crossref_primary_10_1002_advs_202004507
crossref_primary_10_3803_EnM_2021_956
crossref_primary_10_3389_fimmu_2022_772446
crossref_primary_10_1038_s41568_024_00743_1
crossref_primary_10_1038_s41467_022_30757_y
crossref_primary_10_1007_s12272_019_01130_3
crossref_primary_10_1080_00071668_2020_1847253
crossref_primary_10_1007_s00018_020_03748_9
crossref_primary_10_4252_wjsc_v12_i3_222
crossref_primary_10_1080_01480545_2019_1683571
crossref_primary_10_1186_s12933_020_01092_7
crossref_primary_10_3389_fendo_2022_873699
crossref_primary_10_3390_ijms222111578
crossref_primary_10_1089_neu_2019_6421
crossref_primary_10_4093_dmj_2019_0157
crossref_primary_10_1186_s13045_024_01615_9
crossref_primary_10_1002_art_42091
crossref_primary_10_1016_j_yexcr_2021_112522
crossref_primary_10_1038_s42255_021_00368_w
crossref_primary_10_1016_j_cmet_2019_12_005
crossref_primary_10_1016_j_diabres_2019_107823
crossref_primary_10_1016_j_tcb_2021_10_008
crossref_primary_10_1016_j_cytogfr_2020_11_002
crossref_primary_10_1016_j_tem_2022_08_004
crossref_primary_10_3390_ijms20092359
crossref_primary_10_1152_ajplung_00086_2023
crossref_primary_10_1667_RADE_22_00066_1
crossref_primary_10_1172_jci_insight_126551
crossref_primary_10_1080_21505594_2021_1958470
crossref_primary_10_1002_eji_202250242
crossref_primary_10_1002_path_5997
crossref_primary_10_1016_j_brainres_2025_149591
crossref_primary_10_1136_jmedgenet_2019_106598
crossref_primary_10_1097_HJH_0000000000002727
crossref_primary_10_3390_ijms21228879
crossref_primary_10_20900_immunometab20190008
crossref_primary_10_1002_oby_22584
crossref_primary_10_1093_lifemeta_loac032
crossref_primary_10_1186_s12915_021_01181_3
crossref_primary_10_1111_eci_14290
crossref_primary_10_3389_fphar_2021_785220
crossref_primary_10_1172_jci_insight_124522
crossref_primary_10_3390_cells13070637
crossref_primary_10_3390_ijms25137313
crossref_primary_10_1016_j_lfs_2021_119312
crossref_primary_10_7570_jomes24030
crossref_primary_10_12677_acm_2024_14112973
crossref_primary_10_1038_s41574_021_00529_7
crossref_primary_10_3389_fragi_2022_837575
crossref_primary_10_1152_japplphysiol_00519_2024
crossref_primary_10_1002_agm2_12128
crossref_primary_10_3389_fimmu_2023_1165667
crossref_primary_10_3349_ymj_2023_0131
crossref_primary_10_1007_s11684_023_1033_7
crossref_primary_10_3389_fimmu_2022_926373
crossref_primary_10_1016_j_isci_2021_102265
crossref_primary_10_1097_SLA_0000000000005704
crossref_primary_10_4093_dmj_2020_0087
crossref_primary_10_1038_s42003_024_07144_y
crossref_primary_10_3390_nu12123771
crossref_primary_10_3389_fimmu_2021_651656
crossref_primary_10_2174_0113816128318741240611114448
crossref_primary_10_1186_s12885_024_12727_3
crossref_primary_10_1210_clinem_dgab621
crossref_primary_10_1152_ajpendo_00439_2018
crossref_primary_10_7554_eLife_65109
crossref_primary_10_3389_fimmu_2020_00951
crossref_primary_10_1016_j_canlet_2023_216184
crossref_primary_10_4049_jimmunol_2200641
crossref_primary_10_3390_cells12040522
crossref_primary_10_1007_s10522_024_10164_0
crossref_primary_10_1210_endrev_bnab004
crossref_primary_10_3389_fonc_2022_1009948
crossref_primary_10_3389_jpps_2024_13210
crossref_primary_10_5534_wjmh_200163
crossref_primary_10_1016_j_chembiol_2021_02_010
crossref_primary_10_3390_biomedicines10123081
crossref_primary_10_3389_fimmu_2023_1149366
crossref_primary_10_1007_s11154_023_09827_z
crossref_primary_10_1021_acsami_4c15494
crossref_primary_10_1002_adma_202202715
crossref_primary_10_1016_j_dci_2020_103698
crossref_primary_10_3390_biomedicines9010052
crossref_primary_10_1016_j_arr_2020_101143
crossref_primary_10_1007_s00125_019_05082_7
crossref_primary_10_2147_JHC_S471239
crossref_primary_10_3390_cancers16234081
crossref_primary_10_1111_acel_13195
crossref_primary_10_1089_aid_2020_0067
crossref_primary_10_1155_2021_9980877
crossref_primary_10_1111_jcmm_17725
crossref_primary_10_1016_j_isci_2021_103448
crossref_primary_10_1080_17446651_2024_2307526
crossref_primary_10_1111_os_13993
crossref_primary_10_1016_j_molmet_2022_101642
crossref_primary_10_1016_j_bbamcr_2023_119626
crossref_primary_10_1093_biolre_ioae041
crossref_primary_10_3390_biomedicines11092558
crossref_primary_10_1016_j_yexcr_2020_112010
Cites_doi 10.1155/2015/816460
10.1038/ijo.2014.27
10.1038/nm1451
10.1038/ijo.2015.242
10.1016/j.cmet.2007.06.010
10.1038/nature13895
10.1038/nm.4392
10.1038/nature05894
10.1038/nm.3829
10.1172/JCI200319246
10.1038/nri978
10.1016/j.cmet.2008.04.002
10.1016/j.cmet.2006.05.011
10.1146/annurev-physiol-021909-135846
10.1172/JCI29881
10.1016/j.immuni.2010.05.007
10.1016/j.immuni.2010.11.009
10.1172/JCI90350
10.1111/ggi.12724
10.1084/jem.20080452
10.1172/JCI31422
10.1182/blood-2016-01-696617
10.1161/CIRCRESAHA.110.216523
10.1146/annurev-pathol-011110-130138
10.1172/JCI200319451
10.1016/j.immuni.2013.04.001
10.4049/jimmunol.0901698
10.1371/journal.pone.0024358
10.2337/db11-0860
10.1038/nm.4394
10.1371/journal.pone.0086541
10.1038/ncomms5732
10.1038/nature24042
10.1073/pnas.94.21.11514
10.1007/s00125-015-3506-y
10.1038/nri3088
10.1038/srep44351
10.1016/j.cmet.2012.06.012
10.1002/jcsm.12169
10.1016/j.molbiopara.2005.09.009
10.1128/MCB.20.10.3742-3751.2000
10.1038/nrendo.2015.189
10.1161/01.RES.0000202804.84885.d0
10.1038/sj.emboj.7601986
10.1093/ecco-jcc/jjw013
10.1038/nm.4393
10.1038/ni.2956
10.1016/j.carpath.2012.02.003
10.1371/journal.pone.0148709
10.1016/j.yjmcc.2016.02.014
10.4049/jimmunol.181.6.3733
10.1097/00041433-200310000-00006
10.1007/8904_2015_436
10.1016/j.cmet.2008.04.003
10.1002/oby.20638
10.1083/jcb.201607110
10.12703/P6-13
10.3390/ijms18050986
10.1111/j.1365-2249.2005.02934.x
ContentType Journal Article
Copyright The Author(s) 2018
2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: The Author(s) 2018
– notice: 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID C6C
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7QL
7QP
7QR
7SN
7SS
7ST
7T5
7T7
7TM
7TO
7X7
7XB
88E
8AO
8FD
8FE
8FG
8FH
8FI
8FJ
8FK
ABUWG
AEUYN
AFKRA
ARAPS
AZQEC
BBNVY
BENPR
BGLVJ
BHPHI
C1K
CCPQU
DWQXO
FR3
FYUFA
GHDGH
GNUQQ
H94
HCIFZ
K9.
LK8
M0S
M1P
M7P
P5Z
P62
P64
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQGLB
PQQKQ
PQUKI
PRINS
RC3
SOI
7X8
5PM
ADTOC
UNPAY
DOA
DOI 10.1038/s41467-018-03998-z
DatabaseName Springer Nature OA Free Journals
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
Bacteriology Abstracts (Microbiology B)
Calcium & Calcified Tissue Abstracts
Chemoreception Abstracts
Ecology Abstracts
Entomology Abstracts (Full archive)
Environment Abstracts
Immunology Abstracts
Industrial and Applied Microbiology Abstracts (Microbiology A)
Nucleic Acids Abstracts
Oncogenes and Growth Factors Abstracts
ProQuest Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
ProQuest Pharma Collection
Technology Research Database
ProQuest SciTech Collection
ProQuest Technology Collection
ProQuest Natural Science Journals
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest One Sustainability (subscription)
ProQuest Central UK/Ireland
Advanced Technologies & Computer Science Collection
ProQuest Central Essentials
Biological Science Collection (subscription)
ProQuest Central
Technology Collection
ProQuest Natural Science Collection
Environmental Sciences and Pollution Management
ProQuest One Community College
ProQuest Central
Engineering Research Database
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Central Student
AIDS and Cancer Research Abstracts
SciTech Premium Collection
ProQuest Health & Medical Complete (Alumni)
Biological Sciences
Health & Medical Collection (Alumni Edition)
Medical Database
ProQuest Biological Science Database
AAdvanced Technologies & Aerospace Database (subscription)
ProQuest Advanced Technologies & Aerospace Collection
Biotechnology and BioEngineering Abstracts
ProQuest Central Premium
ProQuest One Academic
Publicly Available Content Database (subscription)
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Applied & Life Sciences
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
Genetics Abstracts
Environment Abstracts
MEDLINE - Academic
PubMed Central (Full Participant titles)
Unpaywall for CDI: Periodical Content
Unpaywall
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest Central Student
Oncogenes and Growth Factors Abstracts
ProQuest Advanced Technologies & Aerospace Collection
ProQuest Central Essentials
Nucleic Acids Abstracts
SciTech Premium Collection
ProQuest Central China
Environmental Sciences and Pollution Management
ProQuest One Applied & Life Sciences
ProQuest One Sustainability
Health Research Premium Collection
Natural Science Collection
Health & Medical Research Collection
Biological Science Collection
Chemoreception Abstracts
Industrial and Applied Microbiology Abstracts (Microbiology A)
ProQuest Central (New)
ProQuest Medical Library (Alumni)
Advanced Technologies & Aerospace Collection
ProQuest Biological Science Collection
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
ProQuest Technology Collection
Health Research Premium Collection (Alumni)
Biological Science Database
Ecology Abstracts
ProQuest Hospital Collection (Alumni)
Biotechnology and BioEngineering Abstracts
Entomology Abstracts
ProQuest Health & Medical Complete
ProQuest One Academic UKI Edition
Engineering Research Database
ProQuest One Academic
Calcium & Calcified Tissue Abstracts
ProQuest One Academic (New)
Technology Collection
Technology Research Database
ProQuest One Academic Middle East (New)
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Natural Science Collection
ProQuest Pharma Collection
ProQuest Central
ProQuest Health & Medical Research Collection
Genetics Abstracts
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
Bacteriology Abstracts (Microbiology B)
AIDS and Cancer Research Abstracts
ProQuest SciTech Collection
Advanced Technologies & Aerospace Database
ProQuest Medical Library
Immunology Abstracts
Environment Abstracts
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database
MEDLINE
CrossRef


MEDLINE - Academic

Database_xml – sequence: 1
  dbid: C6C
  name: Springer Nature OA Free Journals
  url: http://www.springeropen.com/
  sourceTypes: Publisher
– sequence: 2
  dbid: DOA
  name: DOAJ Open Access Full Text
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 3
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 4
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 5
  dbid: UNPAY
  name: Unpaywall
  url: https://proxy.k.utb.cz/login?url=https://unpaywall.org/
  sourceTypes: Open Access Repository
– sequence: 6
  dbid: 8FG
  name: ProQuest Technology Collection
  url: https://search.proquest.com/technologycollection1
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 2041-1723
EndPage 15
ExternalDocumentID oai_doaj_org_article_e543088fca854de18576144178eee3f2
10.1038/s41467-018-03998-z
PMC5908799
29674655
10_1038_s41467_018_03998_z
Genre Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: NIA NIH HHS
  grantid: R01 AG043930
GroupedDBID ---
0R~
39C
3V.
53G
5VS
70F
7X7
88E
8AO
8FE
8FG
8FH
8FI
8FJ
AAHBH
AAJSJ
ABUWG
ACGFO
ACGFS
ACIWK
ACMJI
ACPRK
ACSMW
ADBBV
ADFRT
ADMLS
ADRAZ
AENEX
AEUYN
AFKRA
AFRAH
AHMBA
AJTQC
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AMTXH
AOIJS
ARAPS
ASPBG
AVWKF
AZFZN
BAPOH
BBNVY
BCNDV
BENPR
BGLVJ
BHPHI
BPHCQ
BVXVI
C6C
CCPQU
DIK
EBLON
EBS
EE.
EMOBN
F5P
FEDTE
FYUFA
GROUPED_DOAJ
HCIFZ
HMCUK
HVGLF
HYE
HZ~
KQ8
LK8
M1P
M48
M7P
M~E
NAO
O9-
OK1
P2P
P62
PIMPY
PQQKQ
PROAC
PSQYO
RNS
RNT
RNTTT
RPM
SNYQT
SV3
TSG
UKHRP
AASML
AAYXX
CITATION
PUEGO
CGR
CUY
CVF
ECM
EIF
NPM
PHGZT
7QL
7QP
7QR
7SN
7SS
7ST
7T5
7T7
7TM
7TO
7XB
8FD
8FK
AZQEC
C1K
DWQXO
FR3
GNUQQ
H94
K9.
P64
PHGZM
PJZUB
PKEHL
PPXIY
PQEST
PQGLB
PQUKI
PRINS
RC3
SOI
7X8
5PM
4.4
ADTOC
AFFHD
CAG
COF
EJD
LGEZI
LOTEE
NADUK
NXXTH
UNPAY
ID FETCH-LOGICAL-c606t-f849683c7f6bc57cd31458306c8737e37fd6a58f0a53426305133d93572ce53
IEDL.DBID M48
ISSN 2041-1723
IngestDate Fri Oct 03 12:41:50 EDT 2025
Wed Oct 29 11:45:07 EDT 2025
Tue Sep 30 16:38:47 EDT 2025
Thu Sep 04 20:19:46 EDT 2025
Tue Oct 07 06:35:13 EDT 2025
Thu Apr 03 07:00:28 EDT 2025
Wed Oct 01 03:02:23 EDT 2025
Thu Apr 24 22:58:56 EDT 2025
Fri Feb 21 02:39:57 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Language English
License Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
cc-by
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c606t-f849683c7f6bc57cd31458306c8737e37fd6a58f0a53426305133d93572ce53
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0002-3977-1510
OpenAccessLink https://doaj.org/article/e543088fca854de18576144178eee3f2
PMID 29674655
PQID 2027570094
PQPubID 546298
PageCount 15
ParticipantIDs doaj_primary_oai_doaj_org_article_e543088fca854de18576144178eee3f2
unpaywall_primary_10_1038_s41467_018_03998_z
pubmedcentral_primary_oai_pubmedcentral_nih_gov_5908799
proquest_miscellaneous_2028961580
proquest_journals_2027570094
pubmed_primary_29674655
crossref_primary_10_1038_s41467_018_03998_z
crossref_citationtrail_10_1038_s41467_018_03998_z
springer_journals_10_1038_s41467_018_03998_z
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2018-04-19
PublicationDateYYYYMMDD 2018-04-19
PublicationDate_xml – month: 04
  year: 2018
  text: 2018-04-19
  day: 19
PublicationDecade 2010
PublicationPlace London
PublicationPlace_xml – name: London
– name: England
PublicationTitle Nature communications
PublicationTitleAbbrev Nat Commun
PublicationTitleAlternate Nat Commun
PublicationYear 2018
Publisher Nature Publishing Group UK
Nature Publishing Group
Nature Portfolio
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
– name: Nature Portfolio
References Lumeng, Bodzin, Saltiel (CR14) 2007; 117
Kang (CR13) 2008; 7
Odegaard (CR17) 2008; 7
Kwon (CR59) 2008; 27
Szanto (CR24) 2010; 33
Cao (CR21) 2016; 92
Chung (CR50) 2017; 216
Emmerson (CR55) 2017; 23
Martinez, Gordon (CR44) 2014; 6
Simovic Markovic (CR38) 2016; 10
Oh, Morinaga, Talukdar, Bae, Olefsky (CR40) 2012; 61
Hsiao (CR60) 2000; 20
Chinetti, Fruchart, Staels (CR23) 2003; 14
Feng (CR36) 2011; 6
Kim (CR20) 2012; 16
Odegaard, Chawla (CR12) 2011; 6
Wang, Chrysovergis, Kosak, Eling (CR46) 2014; 22
Dalmas (CR18) 2015; 21
Kim (CR51) 2015; 58
Vats (CR19) 2006; 4
Roszer (CR25) 2015; 2015
Tsai, Lin, Brown, Salis, Breit (CR58) 2016; 40
Ying (CR37) 2017; 127
Chawla (CR43) 2010; 106
Yang (CR54) 2017; 23
Olefsky, Glass (CR4) 2010; 72
Fujita, Taniguchi, Shinkai, Tanaka, Ito (CR47) 2016; 16
Gordon (CR10) 2003; 3
Borner (CR57) 2017; 8
Porcheray (CR6) 2005; 142
Sahoo, Alekseev, Obertas, Nurieva (CR41) 2014; 5
Rodriguez-Prados (CR16) 2010; 185
Xu (CR33) 2006; 98
Artz, Butz, Vestweber (CR34) 2016; 128
Huang (CR15) 2014; 15
Benoit, Desnues, Mege (CR9) 2008; 181
Xu (CR3) 2003; 112
CR56
Lawrence, Natoli (CR7) 2011; 11
Chrysovergis (CR28) 2014; 38
Gordon, Martinez (CR30) 2010; 32
Junttila (CR31) 2008; 205
Weisberg (CR1) 2003; 112
Anthony (CR5) 2006; 12
Koene (CR49) 2015; 24
Phua (CR26) 2017; 7
Lackey, Olefsky (CR2) 2016; 12
Weisser, van Rooijen, Sly (CR35) 2012; 66
Odegaard, Chawla (CR8) 2013; 38
Odegaard (CR11) 2007; 447
Johnen (CR45) 2012; 21
Greber (CR42) 2014; 515
Mullican (CR52) 2017; 23
Montero (CR48) 2016; 11
Hsu (CR53) 2017; 550
Vishwakarma, Anand, Arya, Vats, Bhattacharya (CR29) 2006; 145
Bouhlel (CR22) 2007; 6
Sica, Bronte (CR32) 2007; 117
Bootcov (CR27) 1997; 94
Xie (CR39) 2014; 9
RA Vishwakarma (3998_CR29) 2006; 145
A Sica (3998_CR32) 2007; 117
H Johnen (3998_CR45) 2012; 21
SC Huang (3998_CR15) 2014; 15
G Chinetti (3998_CR23) 2003; 14
Y Fujita (3998_CR47) 2016; 16
E Dalmas (3998_CR18) 2015; 21
JI Odegaard (3998_CR17) 2008; 7
JC Rodriguez-Prados (3998_CR16) 2010; 185
X Wang (3998_CR46) 2014; 22
PJ Emmerson (3998_CR55) 2017; 23
S Gordon (3998_CR10) 2003; 3
A Szanto (3998_CR24) 2010; 33
JI Odegaard (3998_CR11) 2007; 447
BJ Greber (3998_CR42) 2014; 515
S Koene (3998_CR49) 2015; 24
A Artz (3998_CR34) 2016; 128
SB Weisser (3998_CR35) 2012; 66
W Ying (3998_CR37) 2017; 127
L Xie (3998_CR39) 2014; 9
3998_CR56
K Chrysovergis (3998_CR28) 2014; 38
FO Martinez (3998_CR44) 2014; 6
SE Mullican (3998_CR52) 2017; 23
F Porcheray (3998_CR6) 2005; 142
EC Hsiao (3998_CR60) 2000; 20
JI Odegaard (3998_CR12) 2011; 6
L Yang (3998_CR54) 2017; 23
A Chawla (3998_CR43) 2010; 106
JM Olefsky (3998_CR4) 2010; 72
JI Odegaard (3998_CR8) 2013; 38
A Sahoo (3998_CR41) 2014; 5
T Borner (3998_CR57) 2017; 8
MC Kwon (3998_CR59) 2008; 27
IS Junttila (3998_CR31) 2008; 205
SP Weisberg (3998_CR1) 2003; 112
RM Anthony (3998_CR5) 2006; 12
YK Kim (3998_CR51) 2015; 58
T Phua (3998_CR26) 2017; 7
J Xu (3998_CR33) 2006; 98
K Kang (3998_CR13) 2008; 7
CN Lumeng (3998_CR14) 2007; 117
D Vats (3998_CR19) 2006; 4
MA Bouhlel (3998_CR22) 2007; 6
HK Chung (3998_CR50) 2017; 216
L Cao (3998_CR21) 2016; 92
MR Bootcov (3998_CR27) 1997; 94
M Benoit (3998_CR9) 2008; 181
JY Hsu (3998_CR53) 2017; 550
VW Tsai (3998_CR58) 2016; 40
DY Oh (3998_CR40) 2012; 61
DE Lackey (3998_CR2) 2016; 12
H Xu (3998_CR3) 2003; 112
R Montero (3998_CR48) 2016; 11
T Roszer (3998_CR25) 2015; 2015
B Feng (3998_CR36) 2011; 6
B Simovic Markovic (3998_CR38) 2016; 10
SJ Kim (3998_CR20) 2012; 16
T Lawrence (3998_CR7) 2011; 11
S Gordon (3998_CR30) 2010; 32
References_xml – volume: 2015
  start-page: 816460
  year: 2015
  ident: CR25
  article-title: Understanding the mysterious M2 macrophage through activation markers and effector mechanisms
  publication-title: Mediat. Inflamm.
  doi: 10.1155/2015/816460
– volume: 38
  start-page: 1555
  year: 2014
  end-page: 1564
  ident: CR28
  article-title: NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism
  publication-title: Int. J. Obes.
  doi: 10.1038/ijo.2014.27
– volume: 12
  start-page: 955
  year: 2006
  end-page: 960
  ident: CR5
  article-title: Memory T(H)2 cells induce alternatively activated macrophages to mediate protection against nematode parasites
  publication-title: Nat. Med.
  doi: 10.1038/nm1451
– volume: 40
  start-page: 193
  year: 2016
  end-page: 197
  ident: CR58
  article-title: Anorexia-cachexia and obesity treatment may be two sides of the same coin: role of the TGF-b superfamily cytokine MIC-1/GDF15
  publication-title: Int. J. Obes.
  doi: 10.1038/ijo.2015.242
– volume: 6
  start-page: 137
  year: 2007
  end-page: 143
  ident: CR22
  article-title: PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2007.06.010
– volume: 515
  start-page: 283
  year: 2014
  end-page: 286
  ident: CR42
  article-title: The complete structure of the large subunit of the mammalian mitochondrial ribosome
  publication-title: Nature
  doi: 10.1038/nature13895
– volume: 23
  start-page: 1150
  year: 2017
  end-page: 1157
  ident: CR52
  article-title: GFRAL is the receptor for GDF15 and the ligand promotes weight loss in mice and nonhuman primates
  publication-title: Nat. Med.
  doi: 10.1038/nm.4392
– volume: 447
  start-page: 1116
  year: 2007
  end-page: 1120
  ident: CR11
  article-title: Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance
  publication-title: Nature
  doi: 10.1038/nature05894
– volume: 21
  start-page: 610
  year: 2015
  end-page: 618
  ident: CR18
  article-title: Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity
  publication-title: Nat. Med.
  doi: 10.1038/nm.3829
– volume: 112
  start-page: 1796
  year: 2003
  end-page: 1808
  ident: CR1
  article-title: Obesity is associated with macrophage accumulation in adipose tissue
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI200319246
– volume: 3
  start-page: 23
  year: 2003
  end-page: 35
  ident: CR10
  article-title: Alternative activation of macrophages
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri978
– volume: 7
  start-page: 485
  year: 2008
  end-page: 495
  ident: CR13
  article-title: Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2008.04.002
– volume: 4
  start-page: 13
  year: 2006
  end-page: 24
  ident: CR19
  article-title: Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2006.05.011
– volume: 72
  start-page: 219
  year: 2010
  end-page: 246
  ident: CR4
  article-title: Macrophages, inflammation, and insulin resistance
  publication-title: Annu. Rev. Physiol.
  doi: 10.1146/annurev-physiol-021909-135846
– volume: 117
  start-page: 175
  year: 2007
  end-page: 184
  ident: CR14
  article-title: Obesity induces a phenotypic switch in adipose tissue macrophage polarization
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI29881
– volume: 142
  start-page: 481
  year: 2005
  end-page: 489
  ident: CR6
  article-title: Macrophage activation switching: an asset for the resolution of inflammation
  publication-title: Clin. Exp. Immunol.
– volume: 32
  start-page: 593
  year: 2010
  end-page: 604
  ident: CR30
  article-title: Alternative activation of macrophages: mechanism and functions
  publication-title: Immunity
  doi: 10.1016/j.immuni.2010.05.007
– volume: 33
  start-page: 699
  year: 2010
  end-page: 712
  ident: CR24
  article-title: STAT6 transcription factor is a facilitator of the nuclear receptor PPARgamma-regulated gene expression in macrophages and dendritic cells
  publication-title: Immunity
  doi: 10.1016/j.immuni.2010.11.009
– volume: 127
  start-page: 1019
  year: 2017
  end-page: 1030
  ident: CR37
  article-title: Adipose tissue B2 cells promote insulin resistance through leukotriene LTB4/LTB4R1 signaling
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI90350
– volume: 16
  start-page: 17
  issue: Suppl 1
  year: 2016
  end-page: 29
  ident: CR47
  article-title: Secreted growth differentiation factor 15 as a potential biomarker for mitochondrial dysfunctions in aging and age-related disorders
  publication-title: Geriatr. Gerontol. Int.
  doi: 10.1111/ggi.12724
– volume: 205
  start-page: 2595
  year: 2008
  end-page: 2608
  ident: CR31
  article-title: Tuning sensitivity to IL-4 and IL-13: differential expression of IL-4Ralpha, IL-13Ralpha1, and gammac regulates relative cytokine sensitivity
  publication-title: J. Exp. Med.
  doi: 10.1084/jem.20080452
– volume: 117
  start-page: 1155
  year: 2007
  end-page: 1166
  ident: CR32
  article-title: Altered macrophage differentiation and immune dysfunction in tumor development
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI31422
– volume: 128
  start-page: 529
  year: 2016
  end-page: 541
  ident: CR34
  article-title: GDF-15 inhibits integrin activation and mouse neutrophil recruitment through the ALK-5/TGF-betaRII heterodimer
  publication-title: Blood
  doi: 10.1182/blood-2016-01-696617
– volume: 106
  start-page: 1559
  year: 2010
  end-page: 1569
  ident: CR43
  article-title: Control of macrophage activation and function by PPARs
  publication-title: Circ. Res.
  doi: 10.1161/CIRCRESAHA.110.216523
– volume: 6
  start-page: 275
  year: 2011
  end-page: 297
  ident: CR12
  article-title: Alternative macrophage activation and metabolism
  publication-title: Annu. Rev. Pathol.
  doi: 10.1146/annurev-pathol-011110-130138
– volume: 112
  start-page: 1821
  year: 2003
  end-page: 1830
  ident: CR3
  article-title: Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI200319451
– volume: 38
  start-page: 644
  year: 2013
  end-page: 654
  ident: CR8
  article-title: The immune system as a sensor of the metabolic state
  publication-title: Immunity
  doi: 10.1016/j.immuni.2013.04.001
– volume: 185
  start-page: 605
  year: 2010
  end-page: 614
  ident: CR16
  article-title: Substrate fate in activated macrophages: a comparison between innate, classic, and alternative activation
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.0901698
– volume: 6
  start-page: e24358
  year: 2011
  ident: CR36
  article-title: Clodronate liposomes improve metabolic profile and reduce visceral adipose macrophage content in diet-induced obese mice
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0024358
– volume: 61
  start-page: 346
  year: 2012
  end-page: 354
  ident: CR40
  article-title: Increased macrophage migration into adipose tissue in obese mice
  publication-title: Diabetes
  doi: 10.2337/db11-0860
– volume: 23
  start-page: 1158
  year: 2017
  end-page: 1166
  ident: CR54
  article-title: GFRAL is the receptor for GDF15 and is required for the anti-obesity effects of the ligand
  publication-title: Nat. Med.
  doi: 10.1038/nm.4394
– volume: 9
  start-page: e86541
  year: 2014
  ident: CR39
  article-title: Overexpression of IL-10 in C2D macrophages promotes a macrophage phenotypic switch in adipose tissue environments
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0086541
– volume: 5
  year: 2014
  ident: CR41
  article-title: Grail controls Th2 cell development by targeting STAT6 for degradation
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms5732
– volume: 550
  start-page: 255
  year: 2017
  end-page: 259
  ident: CR53
  article-title: Non-homeostatic body weight regulation through a brainstem-restricted receptor for GDF15
  publication-title: Nature
  doi: 10.1038/nature24042
– volume: 94
  start-page: 11514
  year: 1997
  end-page: 11519
  ident: CR27
  article-title: MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-beta superfamily
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.94.21.11514
– volume: 58
  start-page: 771
  year: 2015
  end-page: 780
  ident: CR51
  article-title: Disruption of CR6-interacting factor-1 (CRIF1) in mouse islet beta cells leads to mitochondrial diabetes with progressive beta cell failure
  publication-title: Diabetologia
  doi: 10.1007/s00125-015-3506-y
– volume: 11
  start-page: 750
  year: 2011
  end-page: 761
  ident: CR7
  article-title: Transcriptional regulation of macrophage polarization: enabling diversity with identity
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri3088
– ident: CR56
– volume: 7
  year: 2017
  ident: CR26
  article-title: Angiopoietin-like 4 mediates colonic inflammation by regulating chemokine transcript stability via tristetraprolin
  publication-title: Sci. Rep.
  doi: 10.1038/srep44351
– volume: 16
  start-page: 274
  year: 2012
  end-page: 283
  ident: CR20
  article-title: CRIF1 is essential for the synthesis and insertion of oxidative phosphorylation polypeptides in the mammalian mitochondrial membrane
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2012.06.012
– volume: 8
  start-page: 417
  year: 2017
  end-page: 427
  ident: CR57
  article-title: Anorexia-cachexia syndrome in hepatoma tumour-bearing rats requires the area postrema but not vagal afferents and is paralleled by increased MIC-1/GDF15
  publication-title: J. Cachex. Sarcopenia Muscle
  doi: 10.1002/jcsm.12169
– volume: 145
  start-page: 121
  year: 2006
  end-page: 124
  ident: CR29
  article-title: Glycosylated inositol phospholipid from Entamoeba histolytica: identification and structural characterization
  publication-title: Mol. Biochem. Parasitol.
  doi: 10.1016/j.molbiopara.2005.09.009
– volume: 20
  start-page: 3742
  year: 2000
  end-page: 3751
  ident: CR60
  article-title: Characterization of growth-differentiation factor 15, a transforming growth factor beta superfamily member induced following liver injury
  publication-title: Mol. Cell. Biol.
  doi: 10.1128/MCB.20.10.3742-3751.2000
– volume: 12
  start-page: 15
  year: 2016
  end-page: 28
  ident: CR2
  article-title: Regulation of metabolism by the innate immune system
  publication-title: Nat. Rev. Endocrinol.
  doi: 10.1038/nrendo.2015.189
– volume: 98
  start-page: 342
  year: 2006
  end-page: 350
  ident: CR33
  article-title: GDF15/MIC-1 functions as a protective and antihypertrophic factor released from the myocardium in association with SMAD protein activation
  publication-title: Circ. Res.
  doi: 10.1161/01.RES.0000202804.84885.d0
– volume: 27
  start-page: 642
  year: 2008
  end-page: 653
  ident: CR59
  article-title: Crif1 is a novel transcriptional coactivator of STAT3
  publication-title: EMBO J.
  doi: 10.1038/sj.emboj.7601986
– volume: 10
  start-page: 593
  year: 2016
  end-page: 606
  ident: CR38
  article-title: Galectin-3 plays an important pro-inflammatory role in the induction phase of acute colitis by promoting activation of NLRP3 inflammasome and production of IL-1beta in macrophages
  publication-title: J. Crohn’s Colitis
  doi: 10.1093/ecco-jcc/jjw013
– volume: 23
  start-page: 1215
  year: 2017
  end-page: 1219
  ident: CR55
  article-title: The metabolic effects of GDF15 are mediated by the orphan receptor GFRAL
  publication-title: Nat. Med.
  doi: 10.1038/nm.4393
– volume: 66
  start-page: e4105
  year: 2012
  ident: CR35
  article-title: Depletion and reconstitution of macrophages in mice
  publication-title: J. Vis. Exp.
– volume: 15
  start-page: 846
  year: 2014
  end-page: 855
  ident: CR15
  article-title: Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages
  publication-title: Nat. Immunol.
  doi: 10.1038/ni.2956
– volume: 21
  start-page: 499
  year: 2012
  end-page: 505
  ident: CR45
  article-title: Increased expression of the TGF-b superfamily cytokine MIC-1/GDF15 protects ApoE(-/-) mice from the development of atherosclerosis
  publication-title: Cardiovasc. Pathol.
  doi: 10.1016/j.carpath.2012.02.003
– volume: 11
  start-page: e0148709
  year: 2016
  ident: CR48
  article-title: GDF-15 is elevated in children with mitochondrial diseases and is induced by mitochondrial dysfunction
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0148709
– volume: 92
  start-page: 185
  year: 2016
  end-page: 195
  ident: CR21
  article-title: CARD9 knockout ameliorates myocardial dysfunction associated with high fat diet-induced obesity
  publication-title: J. Mol. Cell. Cardiol.
  doi: 10.1016/j.yjmcc.2016.02.014
– volume: 181
  start-page: 3733
  year: 2008
  end-page: 3739
  ident: CR9
  article-title: Macrophage polarization in bacterial infections
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.181.6.3733
– volume: 14
  start-page: 459
  year: 2003
  end-page: 468
  ident: CR23
  article-title: Peroxisome proliferator-activated receptors: new targets for the pharmacological modulation of macrophage gene expression and function
  publication-title: Curr. Opin. Lipidol.
  doi: 10.1097/00041433-200310000-00006
– volume: 24
  start-page: 69
  year: 2015
  end-page: 81
  ident: CR49
  article-title: Serum GDF15 levels correlate to mitochondrial disease severity and myocardial strain, but not to disease progression in adult m.3243A G carriers
  publication-title: JIMD Rep.
  doi: 10.1007/8904_2015_436
– volume: 7
  start-page: 496
  year: 2008
  end-page: 507
  ident: CR17
  article-title: Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2008.04.003
– volume: 22
  start-page: 1256
  year: 2014
  end-page: 1263
  ident: CR46
  article-title: Lower NLRP3 inflammasome activity in NAG-1 transgenic mice is linked to a resistance to obesity and increased insulin sensitivity
  publication-title: Obesity
  doi: 10.1002/oby.20638
– volume: 216
  start-page: 149
  year: 2017
  end-page: 165
  ident: CR50
  article-title: Growth differentiation factor 15 is a myomitokine governing systemic energy homeostasis
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201607110
– volume: 6
  start-page: 13
  year: 2014
  ident: CR44
  article-title: The M1 and M2 paradigm of macrophage activation: time for reassessment
  publication-title: F1000prime Rep.
  doi: 10.12703/P6-13
– volume: 15
  start-page: 846
  year: 2014
  ident: 3998_CR15
  publication-title: Nat. Immunol.
  doi: 10.1038/ni.2956
– volume: 61
  start-page: 346
  year: 2012
  ident: 3998_CR40
  publication-title: Diabetes
  doi: 10.2337/db11-0860
– volume: 11
  start-page: 750
  year: 2011
  ident: 3998_CR7
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri3088
– volume: 6
  start-page: 275
  year: 2011
  ident: 3998_CR12
  publication-title: Annu. Rev. Pathol.
  doi: 10.1146/annurev-pathol-011110-130138
– volume: 117
  start-page: 175
  year: 2007
  ident: 3998_CR14
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI29881
– volume: 145
  start-page: 121
  year: 2006
  ident: 3998_CR29
  publication-title: Mol. Biochem. Parasitol.
  doi: 10.1016/j.molbiopara.2005.09.009
– volume: 14
  start-page: 459
  year: 2003
  ident: 3998_CR23
  publication-title: Curr. Opin. Lipidol.
  doi: 10.1097/00041433-200310000-00006
– volume: 16
  start-page: 17
  issue: Suppl 1
  year: 2016
  ident: 3998_CR47
  publication-title: Geriatr. Gerontol. Int.
  doi: 10.1111/ggi.12724
– volume: 6
  start-page: 13
  year: 2014
  ident: 3998_CR44
  publication-title: F1000prime Rep.
  doi: 10.12703/P6-13
– volume: 21
  start-page: 499
  year: 2012
  ident: 3998_CR45
  publication-title: Cardiovasc. Pathol.
  doi: 10.1016/j.carpath.2012.02.003
– volume: 185
  start-page: 605
  year: 2010
  ident: 3998_CR16
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.0901698
– volume: 94
  start-page: 11514
  year: 1997
  ident: 3998_CR27
  publication-title: Proc. Natl Acad. Sci. USA
  doi: 10.1073/pnas.94.21.11514
– volume: 92
  start-page: 185
  year: 2016
  ident: 3998_CR21
  publication-title: J. Mol. Cell. Cardiol.
  doi: 10.1016/j.yjmcc.2016.02.014
– volume: 23
  start-page: 1158
  year: 2017
  ident: 3998_CR54
  publication-title: Nat. Med.
  doi: 10.1038/nm.4394
– volume: 112
  start-page: 1821
  year: 2003
  ident: 3998_CR3
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI200319451
– volume: 72
  start-page: 219
  year: 2010
  ident: 3998_CR4
  publication-title: Annu. Rev. Physiol.
  doi: 10.1146/annurev-physiol-021909-135846
– volume: 32
  start-page: 593
  year: 2010
  ident: 3998_CR30
  publication-title: Immunity
  doi: 10.1016/j.immuni.2010.05.007
– volume: 38
  start-page: 1555
  year: 2014
  ident: 3998_CR28
  publication-title: Int. J. Obes.
  doi: 10.1038/ijo.2014.27
– volume: 38
  start-page: 644
  year: 2013
  ident: 3998_CR8
  publication-title: Immunity
  doi: 10.1016/j.immuni.2013.04.001
– volume: 2015
  start-page: 816460
  year: 2015
  ident: 3998_CR25
  publication-title: Mediat. Inflamm.
  doi: 10.1155/2015/816460
– volume: 205
  start-page: 2595
  year: 2008
  ident: 3998_CR31
  publication-title: J. Exp. Med.
  doi: 10.1084/jem.20080452
– volume: 12
  start-page: 15
  year: 2016
  ident: 3998_CR2
  publication-title: Nat. Rev. Endocrinol.
  doi: 10.1038/nrendo.2015.189
– volume: 117
  start-page: 1155
  year: 2007
  ident: 3998_CR32
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI31422
– volume: 7
  start-page: 485
  year: 2008
  ident: 3998_CR13
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2008.04.002
– volume: 20
  start-page: 3742
  year: 2000
  ident: 3998_CR60
  publication-title: Mol. Cell. Biol.
  doi: 10.1128/MCB.20.10.3742-3751.2000
– volume: 5
  year: 2014
  ident: 3998_CR41
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms5732
– volume: 106
  start-page: 1559
  year: 2010
  ident: 3998_CR43
  publication-title: Circ. Res.
  doi: 10.1161/CIRCRESAHA.110.216523
– volume: 16
  start-page: 274
  year: 2012
  ident: 3998_CR20
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2012.06.012
– volume: 181
  start-page: 3733
  year: 2008
  ident: 3998_CR9
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.181.6.3733
– volume: 8
  start-page: 417
  year: 2017
  ident: 3998_CR57
  publication-title: J. Cachex. Sarcopenia Muscle
  doi: 10.1002/jcsm.12169
– volume: 4
  start-page: 13
  year: 2006
  ident: 3998_CR19
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2006.05.011
– volume: 6
  start-page: 137
  year: 2007
  ident: 3998_CR22
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2007.06.010
– volume: 3
  start-page: 23
  year: 2003
  ident: 3998_CR10
  publication-title: Nat. Rev. Immunol.
  doi: 10.1038/nri978
– volume: 58
  start-page: 771
  year: 2015
  ident: 3998_CR51
  publication-title: Diabetologia
  doi: 10.1007/s00125-015-3506-y
– volume: 27
  start-page: 642
  year: 2008
  ident: 3998_CR59
  publication-title: EMBO J.
  doi: 10.1038/sj.emboj.7601986
– volume: 33
  start-page: 699
  year: 2010
  ident: 3998_CR24
  publication-title: Immunity
  doi: 10.1016/j.immuni.2010.11.009
– volume: 66
  start-page: e4105
  year: 2012
  ident: 3998_CR35
  publication-title: J. Vis. Exp.
– volume: 40
  start-page: 193
  year: 2016
  ident: 3998_CR58
  publication-title: Int. J. Obes.
  doi: 10.1038/ijo.2015.242
– volume: 21
  start-page: 610
  year: 2015
  ident: 3998_CR18
  publication-title: Nat. Med.
  doi: 10.1038/nm.3829
– volume: 127
  start-page: 1019
  year: 2017
  ident: 3998_CR37
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI90350
– ident: 3998_CR56
  doi: 10.3390/ijms18050986
– volume: 9
  start-page: e86541
  year: 2014
  ident: 3998_CR39
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0086541
– volume: 216
  start-page: 149
  year: 2017
  ident: 3998_CR50
  publication-title: J. Cell Biol.
  doi: 10.1083/jcb.201607110
– volume: 6
  start-page: e24358
  year: 2011
  ident: 3998_CR36
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0024358
– volume: 12
  start-page: 955
  year: 2006
  ident: 3998_CR5
  publication-title: Nat. Med.
  doi: 10.1038/nm1451
– volume: 142
  start-page: 481
  year: 2005
  ident: 3998_CR6
  publication-title: Clin. Exp. Immunol.
  doi: 10.1111/j.1365-2249.2005.02934.x
– volume: 128
  start-page: 529
  year: 2016
  ident: 3998_CR34
  publication-title: Blood
  doi: 10.1182/blood-2016-01-696617
– volume: 447
  start-page: 1116
  year: 2007
  ident: 3998_CR11
  publication-title: Nature
  doi: 10.1038/nature05894
– volume: 98
  start-page: 342
  year: 2006
  ident: 3998_CR33
  publication-title: Circ. Res.
  doi: 10.1161/01.RES.0000202804.84885.d0
– volume: 23
  start-page: 1150
  year: 2017
  ident: 3998_CR52
  publication-title: Nat. Med.
  doi: 10.1038/nm.4392
– volume: 7
  start-page: 496
  year: 2008
  ident: 3998_CR17
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2008.04.003
– volume: 24
  start-page: 69
  year: 2015
  ident: 3998_CR49
  publication-title: JIMD Rep.
  doi: 10.1007/8904_2015_436
– volume: 23
  start-page: 1215
  year: 2017
  ident: 3998_CR55
  publication-title: Nat. Med.
  doi: 10.1038/nm.4393
– volume: 11
  start-page: e0148709
  year: 2016
  ident: 3998_CR48
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0148709
– volume: 550
  start-page: 255
  year: 2017
  ident: 3998_CR53
  publication-title: Nature
  doi: 10.1038/nature24042
– volume: 7
  year: 2017
  ident: 3998_CR26
  publication-title: Sci. Rep.
  doi: 10.1038/srep44351
– volume: 10
  start-page: 593
  year: 2016
  ident: 3998_CR38
  publication-title: J. Crohn’s Colitis
  doi: 10.1093/ecco-jcc/jjw013
– volume: 112
  start-page: 1796
  year: 2003
  ident: 3998_CR1
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI200319246
– volume: 515
  start-page: 283
  year: 2014
  ident: 3998_CR42
  publication-title: Nature
  doi: 10.1038/nature13895
– volume: 22
  start-page: 1256
  year: 2014
  ident: 3998_CR46
  publication-title: Obesity
  doi: 10.1002/oby.20638
SSID ssj0000391844
Score 2.5972817
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...
SourceID doaj
unpaywall
pubmedcentral
proquest
pubmed
crossref
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 1551
SubjectTerms 13/21
13/31
13/51
38/109
38/22
38/44
38/77
38/90
631/250/256/2515
692/163/2743/137/773
692/163/2743/2037
692/163/2743/393
Adipose Tissue
Animal models
Animals
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Growth Differentiation Factor 15 - genetics
Growth Differentiation Factor 15 - metabolism
Humanities and Social Sciences
Insulin
Insulin Resistance
Interleukin 4
Interleukin-4 - genetics
Interleukin-4 - metabolism
Macrophages
Macrophages - metabolism
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mitochondria
Mitochondria - metabolism
multidisciplinary
Obesity - genetics
Obesity - metabolism
Oxidation resistance
Oxidative Phosphorylation
Oxidative Stress
Phosphorylation
Polarization
Rosiglitazone
Science
Science (multidisciplinary)
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3daxQxEB-kUNQH8dvVKiv4ZpduLskmeWyLpQiK-AF9C9l80INzr3h3aPvXO5PdW-9Qqg--JlmYzEdmZif5DcAr7YOWXpJ9M1kJl5rKhbapjGZId0KHJOiB87v3zekX8fZMnm20-qI7YT08cM-4gygFR0tI3mkpQiToIsphmNIxRp7y6Vtrs5FM5TOYG0xdxPBKpub6YCHymVAzelFG78qutjxRBuz_U5T5-2XJsWJ6G26uugt3-d3NZhtO6eQu3BmiyfKw38U9uBG7-7Db95e8fAAfPhIwawzl_Mc0ZITv0qNz9Bh5l9Ou_Oqof9c5niiLErPu1Wy5oOEe3Hnqy-GeOs1RlInq8RA-nbz5fHxaDS0UKo-ZybJKWphGc69S03qpfOCMCqV147XiKnKVQuOkTrWTnKDba2r3EgyXauKj5I9gp5t38QmU0rcYDCrWmloLGZhLjIfaiYlnOmLIUQBbM9P6AV2cmlzMbK5yc217AVgUgM0CsFcFvB6_ueixNa5dfUQyGlcSLnYeQG2xg7bYv2lLAXtrCdvBWBeW_v8QzL8RBbwcp9HMqHbiujhf5TXaYPSncaePe4UYKZmYRhEMXQFqS1W2SN2e6abnGcqbOs4rYwrYXyvVL7KuY8X-qHj_wLmn_4Nzz-DWJBuPqJjZg53lt1V8jvHYsn2RTe8nSlEuew
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1baxQxFD7ULaI-iPeOVhnBNzs4mSST5EHESksRXEpV6FvIJpl2YZ3ZdnfR9tebk7nURVl8TTKQ5FxyMifn-wDeSOsktxztm_CMmarMjJuUmZIkzLsKBxLDAucv4_LoO_t8yk-3YNzXwuCzyt4nRkftGov_yOMlHbHYFfswv8iQNQqzqz2FhumoFdz7CDF2C7YLRMYawfb-wfj4ZPjrgnjokrGueian8t2CRV-RE6w0w3qz67UTKgL5_yv6_PsR5ZBJvQd3VvXcXP00s9kfh9XhA7jfRZnpx1YtHsKWrx_B7ZZ38uoxHJ8gYKt3afNr6iLyd2rDoWlDRJ5O6_SHQV6v8-BpFmm4ja9mywU2t6DPU5t279exD6PPoDZP4OvhwbdPR1lHrZDZcGNZZpVkqpTUiqqcWC6sowQTqHlppaDCU1G50nBZ5YZThHTPkQbGKcpFYT2nT2FUN7XfgZTbSQgSBZmoXDLuiKkIdblhhSXSh1AkAdJvprYd6jiSX8x0zH5TqVsB6CAAHQWgrxN4O3wzbzE3No7eRxkNIxEvOzY0l2e6Mz_tOaPBn1bWSM6cRwAsvAkTIb33tCoS2O0lrDsjXugblUvg9dAdzA9zKqb2zSqOkSpEhTKs9FmrEMNMClUKhKdLQKypytpU13vq6XmE-EYmeqFUAnu9Ut1Ma9NW7A2K9x8793zzol_A3SKaBcuI2oXR8nLlX4YIbDl51ZnVb2I7LPY
  priority: 102
  providerName: ProQuest
– databaseName: Springer Nature HAS Fully OA
  dbid: AAJSJ
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3di9QwEB_OPUR9EL-tnlLBN7fYtEmTPK7icSwo4incW0iTlFvY6x7uLnr31zuTdqvl5NDXJinT-ehMMpnfALxWzivhBNk3Exm3TZVZX1eZVgzpbtAhcSpw_vipOvrG5yfiZA-mu1qYUf4-QneveTTmnFEpGBWEXd6AfYWKqSawP5vNj-fDmQqhnSvO-9oYXP726uKR_4kw_X-LLa9ekRzypHfg1rY9txc_7HL5hys6vAd3-xgynXVCvw97oX0AN7uukhcP4fMXgmMNPl39XPiI6506dIkO4-100aZnlrp2neJ_ZJ3iXnu73KzpcQfpvHBpfzudxii2RKV4BMeHH76-P8r6xgmZw_3IJmsU15UqnWyq2gnpfMkoPZpXDvkmQykbX1mhmtyKkgDbc2ry4nUpZOGCKB_DpF214SmkwtUYAkpW61xx4ZltWOlzywvHVMBAIwG2Y6ZxPaY4tbZYmpjbLpXpBGBQACYKwFwm8GZYc94halw7-x3JaJhJaNjxASqJ6Y3LBMFRHVTjrBLcB4K3on0ukyqEUDZFAgc7CZveRNeGTn0I3F_zBF4Nw2hclDGxbVht4xylMeZT-KVPOoUYKCl0JQl8LgE5UpURqeORdnEaAbypz7zUOoHpTql-k3UdK6aD4v0D557939ufw-0imgnPmD6Ayeb7NrzAeGtTv-zN7BdW9CHT
  priority: 102
  providerName: Springer Nature
– databaseName: Unpaywall
  dbid: UNPAY
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1Lb9QwEB6VrRDlwLsQKChI3GiWOLZj51gQVYVEVQEV5RQ5ftAVS3bV3Qi6vx6P84CFqqLXeCzZ47HnczzzDcALqY3kmuP-JjxhyuWJMlWeFJL4cTvvkBgmOL8_zA-O2bsTfrIBeZ8LE4L2A6VlOKb76LBXCxa2dEowIQzTwlbjuXHXYDPnHoOPYPP48GjvC1aSSxlJvFemXYZMSuUFnde8UCDrvwhh_hsoObyW3oQbTT1X5z_UdPqHQ9q_DZ_7qbRxKN_GzbIa69VfLI9Xn-sduNVh1HivlbwLG7a-B9fbqpXn9-HoA9K9WhPPfk5M4A2PtXe52uP5eFLH3xVWBTv159Qi9nf5Zrpc4OeWMnqi4y76HdsQu3qjewAf999-enOQdIUZEu3vO8vESVbkkmrh8kpzoQ0l-Pya5loKKiwVzuSKS5cqTpEQPsUiMqagXGTacroNo3pW20cQc115iClIVaSScUOUI9SkimWaSOuBTASkX6ZSd5zlWDpjWoa3cyrLVlel11UZdFWuIng59Jm3jB2XSr_G1R8kkW07fJidfS27FSktZ9Sfxk4ryZmxSJ-F92gipLWWuiyCnd52yu4IWJT4VwmLBxQsgudDs9-8-CKjajtrgowsPKaUfqYPW1MbRpIVuUByuwjEmhGuDXW9pZ6cBoJwrGMviiKC3d5cfw_rMlXsDib9H5p7fDXxJ7CVBYtmCSl2YLQ8a-xTj-eW1bNu8_4CkZlEsQ
  priority: 102
  providerName: Unpaywall
Title Reduced oxidative capacity in macrophages results in systemic insulin resistance
URI https://link.springer.com/article/10.1038/s41467-018-03998-z
https://www.ncbi.nlm.nih.gov/pubmed/29674655
https://www.proquest.com/docview/2027570094
https://www.proquest.com/docview/2028961580
https://pubmed.ncbi.nlm.nih.gov/PMC5908799
https://www.nature.com/articles/s41467-018-03998-z.pdf
https://doaj.org/article/e543088fca854de18576144178eee3f2
UnpaywallVersion publishedVersion
Volume 9
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAFT
  databaseName: Open Access Digital Library
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: KQ8
  dateStart: 20150101
  isFulltext: true
  titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html
  providerName: Colorado Alliance of Research Libraries
– providerCode: PRVAON
  databaseName: DOAJ Open Access Full Text
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: DOA
  dateStart: 20150101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVEBS
  databaseName: Inspec with Full Text
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: ADMLS
  dateStart: 20121101
  isFulltext: true
  titleUrlDefault: https://www.ebsco.com/products/research-databases/inspec-full-text
  providerName: EBSCOhost
– providerCode: PRVBFR
  databaseName: Free Medical Journals
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: DIK
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: http://www.freemedicaljournals.com
  providerName: Flying Publisher
– providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: M~E
  dateStart: 20100101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVAQN
  databaseName: PubMed Central
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: RPM
  dateStart: 20120101
  isFulltext: true
  titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/
  providerName: National Library of Medicine
– providerCode: PRVAQT
  databaseName: Springer Nature - nature.com Journals - Fully Open Access
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: NAO
  dateStart: 20101201
  isFulltext: true
  titleUrlDefault: https://www.nature.com/siteindex/index.html
  providerName: Nature Publishing
– providerCode: PRVPQU
  databaseName: ProQuest Technology Collection
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: 8FG
  dateStart: 20100401
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/technologycollection1
  providerName: ProQuest
– providerCode: PRVFZP
  databaseName: Scholars Portal Journals: Open Access
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 20250131
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: M48
  dateStart: 20101001
  isFulltext: true
  titleUrlDefault: http://journals.scholarsportal.info
  providerName: Scholars Portal
– providerCode: PRVAVX
  databaseName: Springer Nature HAS Fully OA
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: AAJSJ
  dateStart: 20101201
  isFulltext: true
  titleUrlDefault: https://www.springernature.com
  providerName: Springer Nature
– providerCode: PRVAVX
  databaseName: Springer Nature OA Free Journals
  customDbUrl:
  eissn: 2041-1723
  dateEnd: 99991231
  omitProxy: true
  ssIdentifier: ssj0000391844
  issn: 2041-1723
  databaseCode: C6C
  dateStart: 20101201
  isFulltext: true
  titleUrlDefault: http://www.springeropen.com/
  providerName: Springer Nature
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwELf2IQQ8IL4JjCpIvLFAXNux_YBQV61MlVZVG5XGU-Q6DqtU0tEPse6v5875gIoy8ZJItiM5vjvfXZz7_Qh5q2ymhBVo31RE3ORJZLJxEmlFYd45OCSOBc6ng-RkxPsX4mKH1HRH1QIutqZ2yCc1mk_fX_9YfwKD_1iWjKsPC-7NPaZYLIYlYze7ZB88lUYqh9Mq3Pc7M9OQ0PCqdmb7o4gOrBOJsGIbrsoj-m8LQ__-m7I5Ur1P7q6KK7P-aabTP7xW7yF5UIWbYafUj0dkxxWPyZ2SgHL9hAzPELnVZeHsepJ5CPDQgve0EJqHkyL8bpDg6xK2nEUIaflqulxgc4n-PLFh9SM79mEYCvrzlJz3jr90T6KKYyGykLoso1xxnShmZZ6MrZA2YxRPUuPEKsmkYzLPEiNUHhvBENs9Rj6YTDMh29YJ9ozsFbPCvSChsGOIFiUd61hxkVGTU5bFhrctVQ5ikoDQejFTW8GPIwvGNPXH4EylpSxSkEXqZZHeBORd88xVCb5x6-gjlFEzEoGzfcNs_i2t7DB1gjPYWHNrlOCZQyQsTImpVM45lrcDclBLOK2VMcUPRMgDoHlA3jTdYId4uGIKN1v5MUpDeKjgTZ-XCtHMpFaogMgNVdmY6mZPMbn0WN9ISS-1DshhrVS_p3XbUhw2ivcfK_fynzN-Re61vXHwiOoDsrecr9xriMKW4xbZlRcSrqr3uUX2O53-eR_uR8eD4Rm0dpNuy3_faHkThJ7RYNj5-gt8gDJZ
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1LbxMxEB5VRahwQLzZUmCR4ERXrNf22ntAiFeV0ocQFCknLMf20kjpJjSJSvqb-JF4vI8SgSIuvdpeyfY8PN7xfB_AM2ms5IajfROeMF3mibaDPCkk8fMu_YHEsMD54DDvfWUf-7y_Br_aWhh8Vtn6xOCo7djgP_JwSUcs9oK9nvxIkDUKs6sthUatFntuceavbNNXu--9fJ9n2c6Ho3e9pGEVSIwP1mdJKVmRS2pEmQ8MF8ZSgrnDNDdSUOGoKG2uuSxTzSmimafIgGILykVmHHJEeId_hVHvSbz1iL7o_ugg1rpkrKnMSal8OWXBD6UEq9iwlu186fQLJAH_imz_fqDZZWmvw8a8mujFmR6N_jgId27CjSaCjd_UKncL1lx1G67WnJaLO_DpM4LBOhuPfw5tQBWPjT-QjY_242EVn2jkDDv2Xmwa-5v-fDSbYnMNKD00cfM2HvswsvUqeRe-XMIG34P1aly5BxBzM_ABqCCDIpWMW6JLQm2qWWaIdD7MiYC0m6lMg2iOxBojFTLrVKpaAMoLQAUBqPMIXnTfTGo8j5Wj36KMupGIxR0axqffVWPaynGvDVKWRkvOrENwLbxlEyGdc7TMIthqJawaBzFVF-ocwdOu25s25mt05cbzMEYWPuKUfqX3a4XoZpIVuUDouwjEkqosTXW5pxoeB_hwZLkXRRHBdqtUF9NatRXbneL9x85trl70E9joHR3sq_3dw72HcC0LJsISUmzB-ux07h75SG82eBwMLIZvl2vPvwGEp1_J
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwELaqIl4HxLuBAkGCE40ax3ZsHxACyqqlUFU8pD1hObbTrrQkS3dXZfvL-Hl4nEdZgVZceo0dyfE8PM7MfB9Cz4SxghkG9o1ZQnWZJ9oWeSIF9usu_YFEocH540G--5W-H7LhGvrV9cJAWWXnE4OjtrWBf-Thkg5Y7JJul21ZxOHO4NXkRwIMUpBp7eg0GhXZd4tTf32bvtzb8bJ-nmWDd1_e7iYtw0BifOA-S0pBZS6I4WVeGMaNJRjyiGluBCfcEV7aXDNRppoRQDZPgQ3FSsJ4ZhzwRXjnf4kTIqGYkA95_3cHcNcFpW2XTkrE9pQGn5Ri6GiDvrazpZMwEAb8K8r9u1izz9heR1fn1UQvTvV4_MehOLiJbrTRbPy6Ub9baM1Vt9Hlht9ycQcdfgJgWGfj-ufIBoTx2PjD2fjIPx5V8XcN_GHH3qNNY3_rn49nU3jcgEuPTNzWycMYRLlePe-izxewwffQelVXbgPFzBQ-GOW4kKmgzGJdYmJTTTODhfMhT4Rwt5nKtOjmQLIxViHLToRqBKC8AFQQgDqL0Iv-nUmD7bFy9huQUT8TcLnDg_rkSLVmrhyjxPvt0mjBqHUAtAU3bsyFc46UWYQ2Owmr1llM1blqR-hpP-zNHHI3unL1PMwR0kefwn_p_UYh-pVkMucAgxchvqQqS0tdHqlGxwFKHBjvuZQR2uqU6nxZq7Ziq1e8_9i5B6s_-gm64i1Zfdg72H-IrmXBQmiC5SZan53M3SMf9M2Kx8G-YvTtYs35N2nmZAw
linkToUnpaywall http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1Lb9QwEB6VrRDlwLsQKChI3GiWOLZj51gQVYVEVQEV5RQ5ftAVS3bV3Qi6vx6P84CFqqLXeCzZ47HnczzzDcALqY3kmuP-JjxhyuWJMlWeFJL4cTvvkBgmOL8_zA-O2bsTfrIBeZ8LE4L2A6VlOKb76LBXCxa2dEowIQzTwlbjuXHXYDPnHoOPYPP48GjvC1aSSxlJvFemXYZMSuUFnde8UCDrvwhh_hsoObyW3oQbTT1X5z_UdPqHQ9q_DZ_7qbRxKN_GzbIa69VfLI9Xn-sduNVh1HivlbwLG7a-B9fbqpXn9-HoA9K9WhPPfk5M4A2PtXe52uP5eFLH3xVWBTv159Qi9nf5Zrpc4OeWMnqi4y76HdsQu3qjewAf999-enOQdIUZEu3vO8vESVbkkmrh8kpzoQ0l-Pya5loKKiwVzuSKS5cqTpEQPsUiMqagXGTacroNo3pW20cQc115iClIVaSScUOUI9SkimWaSOuBTASkX6ZSd5zlWDpjWoa3cyrLVlel11UZdFWuIng59Jm3jB2XSr_G1R8kkW07fJidfS27FSktZ9Sfxk4ryZmxSJ-F92gipLWWuiyCnd52yu4IWJT4VwmLBxQsgudDs9-8-CKjajtrgowsPKaUfqYPW1MbRpIVuUByuwjEmhGuDXW9pZ6cBoJwrGMviiKC3d5cfw_rMlXsDib9H5p7fDXxJ7CVBYtmCSl2YLQ8a-xTj-eW1bNu8_4CkZlEsQ
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Reduced+oxidative+capacity+in+macrophages+results+in+systemic+insulin+resistance&rft.jtitle=Nature+communications&rft.au=Jung%2C+Saet-Byel&rft.au=Choi%2C+Min+Jeong&rft.au=Ryu%2C+Dongryeol&rft.au=Yi%2C+Hyon-Seung&rft.date=2018-04-19&rft.eissn=2041-1723&rft.volume=9&rft.issue=1&rft.spage=1551&rft_id=info:doi/10.1038%2Fs41467-018-03998-z&rft_id=info%3Apmid%2F29674655&rft.externalDocID=29674655
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2041-1723&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2041-1723&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2041-1723&client=summon