SUMMARY 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.
Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88
Angela Castoldi,Vinícius Andrade-Oliveira,C. F. Aguiar,M. Amano,Jennifer Lee,M. T. Miyagi,Marcela Teatin Latancia,T. Braga,M. B. da Silva,A. Ignacio,J. D. Lima,F. V. Loures,J. Albuquerque,M. B. Macêdo,R. R. Almeida,J. W. Gaiarsa,L. Luévano‐Martínez,Thiago Belchior,M. Hiyane,Gordon D. Brown,M. Mori,C. Hoffmann,M. Seelaender,Willian T. Festuccia,P. M. Moraes-Vieira,N. Câmara
Published 2017 in Cell Reports
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- Publication year
2017
- Venue
Cell Reports
- Publication date
2017-06-13
- Fields of study
Biology, Medicine
- Identifiers
- External record
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Semantic Scholar, PubMed
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