4.8 Article

Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88

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CELL REPORTS
卷 19, 期 11, 页码 2272-2288

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CELL PRESS
DOI: 10.1016/j.celrep.2017.05.059

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资金

  1. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [11/15682-4, 12/02270-2, 15/18121-4]
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [465656/2014-5]
  3. NIH/NIDDK [R01DK106210]
  4. Wellcome Trust [102705]
  5. MRC Centre for Medical Mycology [MR/N006364/1]
  6. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [15/18121-4, 11/15682-4] Funding Source: FAPESP
  7. Medical Research Council [MR/N006364/1] Funding Source: researchfish
  8. 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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