Journal
CELL METABOLISM
Volume 24, Issue 3, Pages 510-519Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2016.08.003
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Funding
- American Diabetes JF Development Award [116JDF061]
- BWH Evergreen Innovation Grant
- BADERC grant
- ERC Stg grant [679173]
- NIH [AI063428, AI028973]
- Health Research Board Ireland
- Canada Research Chairs program
- CIHR [123391]
- BBDC-Novo Nordisk Chair in diabetes research
- [NIHR01111144]
- European Research Council (ERC) [679173] Funding Source: European Research Council (ERC)
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Adipose-resident invariant natural killer T (iNKT) cells are key players in metabolic regulation. iNKT cells are innate lipid sensors, and their activation, using their prototypic ligand alpha-galactosylceramide (alpha GalCer), induces weight loss and restores glycemic control in obesity. Here, iNKT activation induced fibroblast growth factor 21 (FGF21) production and thermogenic browning of white fat. Complete metabolic analysis revealed that iNKT cell activation induced increased body temperature, V02, VC02, and fatty acid oxidation, without affecting food intake or activity. FGF21 induction played a major role in iNKT cell-induced weight loss, as FGF21 null mice lost significantly less weight after aGalCer treatment. The glucagon-like peptide 1 (GLP-1) receptor agonist, liraglutide, also activated iNKT cells in humans and mice. In iNKT-deficient mice, liraglutide promoted satiety but failed to induce FGF21, resulting in less weight loss. These findings reveal an iNKT cell-FGF21 axis that defines a new immune-mediated pathway that could be targeted for glycemic control and weight regulation.
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