|  Help  |  About  |  Contact Us

Publication : GIP regulates inflammation and body weight by restraining myeloid-cell-derived S100A8/A9.

First Author  Mantelmacher FD Year  2019
Journal  Nat Metab Volume  1
Issue  1 Pages  58-69
PubMed ID  32694806 Mgi Jnum  J:294871
Mgi Id  MGI:6453674 Doi  10.1038/s42255-018-0001-z
Citation  Mantelmacher FD, et al. (2019) GIP regulates inflammation and body weight by restraining myeloid-cell-derived S100A8/A9. Nat Metab 1(1):58-69
abstractText  Enteroendocrine cells relay energy-derived signals to immune cells to signal states of nutrient abundance and control immunometabolism. Emerging data suggest that the gut-derived nutrient-induced incretin glucose-dependent insulinotropic polypeptide (GIP) operates at the interface of metabolism and inflammation. Here we show that high-fat diet (HFD)-fed mice with immune cell-targeted GIP receptor (GIPR) deficiency exhibit greater weight gain, insulin resistance, hepatic steatosis and significant myelopoiesis concomitantly with impaired energy expenditure and inguinal white adipose tissue (WAT) beiging. Expression of the S100 calcium-binding protein S100A8 was increased in the WAT of mice with immune cell-targeted GIPR deficiency and co-deletion of GIPR and the heterodimer S100A8/A9 in immune cells ameliorated the aggravated metabolic and inflammatory phenotype following a HFD. Specific GIPR deletion in myeloid cells identified this lineage as the target of GIP effects. Furthermore, GIP directly downregulated S100A8 expression in adipose tissue macrophages. Collectively, our results identify a myeloid-GIPR-S100A8/A9 signalling axis coupling nutrient signals to the control of inflammation and adaptive thermogenesis.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

9 Bio Entities

0 Expression