Journal
CELL REPORTS
Volume 19, Issue 11, Pages 2272-2288Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.05.059
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Funding
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [11/15682-4, 12/02270-2, 15/18121-4]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [465656/2014-5]
- NIH/NIDDK [R01DK106210]
- Wellcome Trust [102705]
- MRC Centre for Medical Mycology [MR/N006364/1]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [15/18121-4, 11/15682-4] Funding Source: FAPESP
- Medical Research Council [MR/N006364/1] Funding Source: researchfish
- MRC [MR/N006364/1] Funding Source: UKRI
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The underlying mechanism by which MyD88 regulates the development of obesity, metainflammation, and insulin resistance (IR) remains unknown. Global deletion of MyD88 in high-fat diet (HFD)fed mice resulted in increased weight gain, impaired glucose homeostasis, elevated Dectin-1 expression in adipose tissue (AT), and proinflammatory CD11c+ AT macrophages (ATMs). Dectin-1 KO mice were protected from diet-induced obesity (DIO) and IR and had reduced CD11c+ AT macrophages. Dectin-1 antagonist improved glucose homeostasis and decreased CD11c+ AT macrophages in chow-and HFD-fed MyD88 KO mice. Dectin-1 agonist worsened glucose homeostasis in MyD88 KO mice. Dectin-1 expression is increased in AT from obese individuals. Together, our data indicate that Dectin-1 regulates AT inflammation by promoting CD11c+ AT macrophages in the absence of MyD88 and identify a role for Dectin-1 in chronic inflammatory states, such as obesity. This suggests that Dectin-1 may have ther-apeutic implications as a biomarker for metabolic dysregulation in humans.
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