Dectin-1 activation exacerbates obesity and insulin resistance in the absence of myD88
Castoldi, Angela; Andrade-Oliveira, Vinicius; Aguiar, Cristhiane Favero; Amano, Mariane Tami; Lee, Jennifer; Miyagi, Marcelli Terumi; Latancia, Marcela Teatin; Braga, Tarcio Teodoro; Silva, Marina Burgos da; Ignacio, Aline; Lima, Joanna Darck Carola Correia; Loures, Flavio V; Albuquerque, Jose Antonio T; Macedo, Marina Barguil; Almeida, Rafael Ribeiro; Gaiarsa, Jonas W; Luevano-Martinez, Luis A; Belchior, Thiago; Hiyane, Meire Ioshie; Brown, Gordon D; Mori, Marcelo A; Hoffmann, Christian; Seelaender, Marilia; Festuccia, Willian T; Moraes-Vieira, Pedro Manoel; Saraiva Camara, Niels Olsen.
Cell Reports
; 19(11): 2272-2288, 2017.
Artículo
en Inglés
| SES-SP, SESSP-IBPROD, SES-SP | ID: but-ib15153
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.
Biblioteca responsable:
BR78.1
Ubicación: BR78.1
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