| First Author | Satoh M | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 28473 | PubMed ID | 27329323 |
| Mgi Jnum | J:253833 | Mgi Id | MGI:6102627 |
| Doi | 10.1038/srep28473 | Citation | Satoh M, et al. (2016) Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice. Sci Rep 6:28473 |
| abstractText | It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely defined. In this study, we have demonstrated that 3T3-L1 adipocytes can present endogenous ligands to NKT cells, leading to IFN-gamma production, which in turn, stimulated 3T3-L1 adipocytes to enhance expression of CD1d and CCL2, and decrease expression of adiponectin. Furthermore, adipocyte-specific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensitivity in mice fed a high-fat diet (HFD). Accordingly, NKT cells were less activated, IFN-gamma production was significantly reduced, and levels of adiponectin were increased in these animals as compared with control mice on HFD. Importantly, macrophage recruitment into the adipose tissue of adipocyte-specific CD1d-deficient mice was significantly blunted. These findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction of inflammation and functional modulation of adipose tissue that leads to obesity. |
