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GRK2 levels in myeloid cells modulate adipose-liver crosstalk in high fat diet-induced obesity.
Cellular and Molecular Life Sciences ( IF 7.014 ) Pub Date : 2020-01-11 , DOI: 10.1007/s00018-019-03442-5
Rocío Vila-Bedmar,Marta Cruces-Sande,Alba C Arcones,Hanneke L D M Willemen,Patricia Prieto,Isabel Moreno-Indias,Daniel Díaz-Rodríguez,Sara Francisco,Rafael I Jaén,Carolina Gutiérrez-Repiso,Cobi J Heijnen,Lisardo Boscá,Manuel Fresno,Annemieke Kavelaars,Federico Mayor,Cristina Murga

Macrophages are key effector cells in obesity-associated inflammation. G protein-coupled receptor kinase 2 (GRK2) is highly expressed in different immune cell types. Using LysM-GRK2+/- mice, we uncover that a reduction of GRK2 levels in myeloid cells prevents the development of glucose intolerance and hyperglycemia after a high fat diet (HFD) through modulation of the macrophage pro-inflammatory profile. Low levels of myeloid GRK2 confer protection against hepatic insulin resistance, steatosis and inflammation. In adipose tissue, pro-inflammatory cytokines are reduced and insulin signaling is preserved. Macrophages from LysM-GRK2+/- mice secrete less pro-inflammatory cytokines when stimulated with lipopolysaccharide (LPS) and their conditioned media has a reduced pathological influence in cultured adipocytes or naïve bone marrow-derived macrophages. Our data indicate that reducing GRK2 levels in myeloid cells, by attenuating pro-inflammatory features of macrophages, has a relevant impact in adipose-liver crosstalk, thus preventing high fat diet-induced metabolic alterations.
更新日期:2020-01-13

 

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