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

• Autor(a) principal: Castoldi, Angela
• Data de Publicação: 2017
• Outros Autores: 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, Carola Correia Lima, Joanna Darck, 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 [UNIFESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: http://dx.doi.org/10.1016/j.celrep.2017.05.059; https://repositorio.unifesp.br/handle/11600/53659

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.