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

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2017
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Castoldi, Angela
Andrade-Oliveira, Vinicius
Aguiar, Cristhiane Favero
Amano, Mariane Tami
Lee, Jennifer
Miyagi, Marcelli Terumi
Latancia, Marcela Teatin
Braga, Tarcio Teodoro
da Silva, Marina Burgos
Ignacio, Aline
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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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Cell Reports. Cambridge, v. 19, n. 11, p. 2272-2288, 2017.
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