| First Author | Castoldi A | Year | 2017 |
| Journal | Cell Rep | Volume | 19 |
| Issue | 11 | Pages | 2272-2288 |
| PubMed ID | 28614714 | Mgi Jnum | J:254026 |
| Mgi Id | MGI:6103405 | Doi | 10.1016/j.celrep.2017.05.059 |
| Citation | Castoldi A, et al. (2017) Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88. Cell Rep 19(11):2272-2288 |
| abstractText | 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 therapeutic implications as a biomarker for metabolic dysregulation in humans. |
