PMID- 34403503
OWN - NLM
STAT- MEDLINE
DCOM- 20211213
LR  - 20221202
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 164
IP  - 4
DP  - 2021 Dec
TI  - IL-20 is involved in obesity by modulation of adipogenesis and macrophage 
      dysregulation.
PG  - 817-833
LID - 10.1111/imm.13403 [doi]
AB  - IL-20 is a proinflammatory cytokine of the IL-10 family and involved in several 
      diseases. However, the regulatory role of IL-20 in obesity is not well 
      understood. We explored the function of IL-20 in the pathogenesis of 
      obesity-induced insulin resistance by ELISA, Western blotting and flow cytometry. 
      The therapeutic potential of IL-20 monoclonal antibody 7E for ameliorating 
      diet-induced obesity was analysed in murine models. Higher serum IL-20 levels 
      were detected in obese patients. It was upregulated in leptin-deficient (ob/ob), 
      leptin-resistant (db/db) and high-fat diet (HFD)-induced murine obesity models. 
      In vitro, IL-20 regulated the adipocyte differentiation and the polarization of 
      bone marrow-derived macrophages into proinflammatory M1 type. It also caused 
      inflammation and macrophage retention in adipose tissues by upregulating TNF-alpha, 
      monocyte chemotactic protein 1 (MCP-1), netrin 1 and unc5b (netrin receptor) 
      expression in macrophages and netrin 1, leptin and MCP-1 in adipocytes. IL-20 
      promoted insulin resistance by inhibiting glucose uptake in mature adipocytes 
      through the SOCS-3 pathway. In HFD-induced obesity in mice, 7E treatment reduced 
      body weight and improved glucose tolerance and insulin sensitivity; it also 
      reduced local inflammation and the number of M1-like macrophages in adipose 
      tissues. We have identified a critical role of IL-20 in obesity-induced 
      inflammation and insulin resistance, and we conclude that IL-20 may be a novel 
      target for treating obesity and insulin resistance in patients with metabolic 
      disorders.
CI  - (c) 2021 John Wiley & Sons Ltd.
FAU - Hsu, Yu-Hsiang
AU  - Hsu YH
AUID- ORCID: 0000-0003-2738-2638
AD  - Institute of Clinical Medicine, College of Medicine, National Cheng Kung 
      University, Tainan, Taiwan.
AD  - Research Center of Clinical Medicine, National Cheng Kung University Hospital, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Wu, Chih-Hsing
AU  - Wu CH
AD  - Department of Family Medicine, National Cheng Kung University Hospital, College 
      of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Chiu, Chiao-Juno
AU  - Chiu CJ
AD  - Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan 
      University, Taipei, Taiwan.
FAU - Chen, Wei-Ting
AU  - Chen WT
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Chang, Yi-Chieh
AU  - Chang YC
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Wabitsch, Martin
AU  - Wabitsch M
AD  - Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and 
      Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
FAU - Chang, Ming-Shi
AU  - Chang MS
AUID- ORCID: 0000-0001-9577-0400
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210830
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Biomarkers)
RN  - 0 (Cytokines)
RN  - 0 (Insulin)
RN  - 0 (Interleukins)
RN  - IY9XDZ35W2 (Glucose)
RN  - U91R7IMG8U (interleukin 20)
SB  - IM
MH  - Adipocytes/metabolism
MH  - *Adipogenesis/genetics
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Animals
MH  - Biomarkers
MH  - Chemotaxis, Leukocyte
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - *Disease Susceptibility
MH  - Female
MH  - Gene Expression
MH  - Glucose/metabolism
MH  - Humans
MH  - Insulin/metabolism
MH  - Interleukins/genetics/*metabolism
MH  - Macrophages/immunology/*metabolism
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Obesity/*etiology/*metabolism/pathology
MH  - Signal Transduction
PMC - PMC8561105
OTO - NOTNLM
OT  - cytokines
OT  - inflammation
OT  - insulin resistance
OT  - interleukin 20
OT  - obesity
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/08/18 06:00
MHDA- 2021/12/15 06:00
PMCR- 2022/12/01
CRDT- 2021/08/17 17:20
PHST- 2021/08/06 00:00 [revised]
PHST- 2021/03/04 00:00 [received]
PHST- 2021/08/07 00:00 [accepted]
PHST- 2021/08/18 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/08/17 17:20 [entrez]
PHST- 2022/12/01 00:00 [pmc-release]
AID - IMM13403 [pii]
AID - 10.1111/imm.13403 [doi]
PST - ppublish
SO  - Immunology. 2021 Dec;164(4):817-833. doi: 10.1111/imm.13403. Epub 2021 Aug 30.