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

• DOI: 10.1016/j.celrep.2017.05.059
• Publication Date: 2017-06-13T22:02:43Z
• Authors: Angela Castoldi; Vinicius Andrade-...; Cristhiane Favero...; Mariane Tami Amano; Jennifer Lee; Marcelli Terumi M...; Marcela Teatin La...; Tarcio Teodoro Braga; Marina Burgos da ...; Aline Ignácio; Joanna Darck Caro...; Flavio V. Loures; José Antonio T. A...; Marina Barguil Ma...; Rafael Ribeiro Al...; Jonas W. Gaiarsa; Luis A. Luévano-M...; Thiago Belchior; Meire Ioshie Hiyane; Gordon D. Brown; Marcelo A. Mori; Christian Hoffmann; Marília Seelaender; Willian T. Festuccia; Pedro Manoel Mora...; Niels Olsen Sarai...
• Keywords: Proinflammatory cytokine; Homeostasis; CD11c

The underlying mechanism by which MyD88 regulates the development of obesity, metainflammation, and insulin resistance (IR) remains unknown. Global deletion in high-fat diet (HFD)-fed mice resulted increased weight gain, impaired glucose homeostasis, elevated Dectin-1 expression adipose tissue (AT), proinflammatory CD11c+ AT macrophages (ATMs). KO were protected from diet-induced obesity (DIO) IR had reduced macrophages. antagonist improved homeostasis decreased chow- HFD-fed mice. agonist worsened is obese individuals. Together, our data indicate that inflammation promoting absence identify a role for chronic inflammatory states, such as obesity. This suggests may have therapeutic implications biomarker metabolic dysregulation humans.