Journal
CELL REPORTS
Volume 18, Issue 10, Pages 2415-2426Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.02.027
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Funding
- Banting and Best Diabetes Centre (BBDC) of the University of Toronto
- Ontario Graduate Scholarship (OGS)
- BBDC
- CIHR Vanier Canada Graduate Studentship
- CIHR [MT-11219]
- CIHR Bone Team grant [TBO-122068]
- CIHRTeam [THC-135238]
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Insulin resistance is a chronic inflammatory condition accompanying obesity or high fat diets that leads to type 2 diabetes. It is hypothesized that lipids and gut bacterial compounds in particular contribute to metabolic inflammation by activating the immune system; however, the receptors detecting these instigators'' of inflammation remain largely undefined. Here, we show that circulating activators of NOD1, a receptor for bacterial peptidoglycan, increase with high fat feeding inmice, suggesting that NOD1 could be a critical sensor leading to metabolic inflammation. Hematopoietic depletion of NOD1 did not prevent weight gain but protected chimeric mice against diet-induced glucose and insulin intolerance. Mechanistically, while macrophage infiltration of adipose tissue persisted, notably these cells were less pro-inflammatory, had lower CXCL1 production, and consequently, lower neutrophil chemoattraction into the tissue. These findings reveal macrophage NOD1 as a cell-specific target to combat diet-induced inflammation past the step of macrophage infiltration, leading to insulin resistance.
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