PMID- 31363171
OWN - NLM
STAT- MEDLINE
DCOM- 20210603
LR  - 20231213
IS  - 2042-0226 (Electronic)
IS  - 1672-7681 (Print)
IS  - 1672-7681 (Linking)
VI  - 17
IP  - 4
DP  - 2020 Apr
TI  - IL-29 promoted obesity-induced inflammation and insulin resistance.
PG  - 369-379
LID - 10.1038/s41423-019-0262-9 [doi]
AB  - Adipocyte-macrophage crosstalk plays a critical role to regulate adipose tissue 
      microenvironment and cause chronic inflammation in the pathogenesis of obesity. 
      Interleukin-29 (IL-29), a member of type 3 interferon family, plays a role in 
      host defenses against microbes, however, little is known about its role in 
      metabolic disorders. We explored the function of IL-29 in the pathogenesis of 
      obesity-induced inflammation and insulin resistance. We found that serum IL-29 
      level was significantly higher in obese patients. IL-29 upregulated IL-1beta, IL-8, 
      and monocyte chemoattractant protein-1 (MCP-1) expression and decreased glucose 
      uptake and insulin sensitivity in human Simpson-Golabi-Behmel syndrome (SGBS) 
      adipocytes through reducing glucose transporter 4 (GLUT4) and AKT signals. In 
      addition, IL-29 promoted monocyte/macrophage migration. Inhibition of IL-29 could 
      reduce inflammatory cytokine production in macrophage-adipocyte coculture system, 
      which mimic an obese microenvironment. In vivo, IL-29 reduced insulin sensitivity 
      and increased the number of peritoneal macrophages in high-fat diet (HFD)-induced 
      obese mice. IL-29 increased M1/M2 macrophage ratio and enhanced MCP-1 expression 
      in adipose tissues of HFD mice. Therefore, we have identified a critical role of 
      IL-29 in obesity-induced inflammation and insulin resistance, and we conclude 
      that IL-29 may be a novel candidate target for treating obesity and insulin 
      resistance in patients with metabolic disorders.
FAU - Lin, Tian-Yu
AU  - Lin TY
AD  - Institute of Clinical Medicine, College of Medicine, National Cheng Kung 
      University, Tainan, Taiwan, China.
FAU - Chiu, Chiao-Juno
AU  - Chiu CJ
AD  - Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan 
      University, Taipei, Taiwan, China.
FAU - Kuan, Chen-Hsiang
AU  - Kuan CH
AD  - Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan 
      University, Taipei, Taiwan, China.
AD  - Division of Plastic Surgery, Department of Surgery, National Taiwan University 
      Hospital, Taipei, Taiwan, China.
FAU - Chen, Fang-Hsu
AU  - Chen FH
AD  - Institute of Clinical Medicine, College of Medicine, National Cheng Kung 
      University, Tainan, Taiwan, China.
FAU - Shen, Yin-Chen
AU  - Shen YC
AD  - Institute of Clinical Medicine, College of Medicine, National Cheng Kung 
      University, Tainan, Taiwan, China.
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, China.
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, China. brianhsu@mail.ncku.edu.tw.
AD  - Clinical Medicine Research Center, National Cheng Kung University Hospital, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan, China. 
      brianhsu@mail.ncku.edu.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190730
PL  - China
TA  - Cell Mol Immunol
JT  - Cellular & molecular immunology
JID - 101242872
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (interferon-lambda, human)
RN  - 0 (IL29 protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Interleukins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Interleukin)
RN  - 9008-11-1 (Interferons)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - Simpson-Golabi-Behmel syndrome
SB  - IM
MH  - Adipocytes/pathology
MH  - Adipose Tissue/pathology
MH  - Animals
MH  - Arrhythmias, Cardiac/pathology
MH  - Cell Differentiation
MH  - Cell Movement
MH  - Chemokine CCL2/metabolism
MH  - Diet, High-Fat
MH  - Genetic Diseases, X-Linked/pathology
MH  - Gigantism/pathology
MH  - Glucose Transporter Type 4/metabolism
MH  - Heart Defects, Congenital/pathology
MH  - Inflammation/blood/*etiology
MH  - *Insulin Resistance
MH  - Intellectual Disability/pathology
MH  - Interferons/blood/*metabolism
MH  - Interleukin-1beta/metabolism
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - Interleukins/blood/*metabolism
MH  - Lipopolysaccharides
MH  - Macrophages/drug effects/metabolism
MH  - Mice, Inbred C57BL
MH  - Mice, Obese
MH  - Obesity/blood/*complications
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Receptors, Interleukin/metabolism
MH  - Up-Regulation
PMC - PMC7109060
OTO - NOTNLM
OT  - cytokine
OT  - inflammation
OT  - insulin resistance
OT  - obesity
COIS- The authors declare no competing interests.
EDAT- 2019/08/01 06:00
MHDA- 2021/06/04 06:00
PMCR- 2019/07/30
CRDT- 2019/08/01 06:00
PHST- 2019/01/14 00:00 [received]
PHST- 2019/07/01 00:00 [accepted]
PHST- 2019/08/01 06:00 [pubmed]
PHST- 2021/06/04 06:00 [medline]
PHST- 2019/08/01 06:00 [entrez]
PHST- 2019/07/30 00:00 [pmc-release]
AID - 10.1038/s41423-019-0262-9 [pii]
AID - 262 [pii]
AID - 10.1038/s41423-019-0262-9 [doi]
PST - ppublish
SO  - Cell Mol Immunol. 2020 Apr;17(4):369-379. doi: 10.1038/s41423-019-0262-9. Epub 
      2019 Jul 30.