| First Author | Vila-Bedmar R | Year | 2020 |
| Journal | Cell Mol Life Sci | Volume | 77 |
| Issue | 23 | Pages | 4957-4976 |
| PubMed ID | 31927610 | Mgi Jnum | J:313183 |
| Mgi Id | MGI:6791532 | Doi | 10.1007/s00018-019-03442-5 |
| Citation | Vila-Bedmar R, et al. (2020) GRK2 levels in myeloid cells modulate adipose-liver crosstalk in high fat diet-induced obesity. Cell Mol Life Sci 77(23):4957-4976 |
| abstractText | 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 naive 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. |
