| First Author | Mantell BS | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 6 | Pages | e19831 |
| PubMed ID | 21674035 | Mgi Jnum | J:174137 |
| Mgi Id | MGI:5051985 | Doi | 10.1371/journal.pone.0019831 |
| Citation | Mantell BS, et al. (2011) Mice Lacking NKT Cells but with a Complete Complement of CD8 T-Cells Are Not Protected against the Metabolic Abnormalities of Diet-Induced Obesity. PLoS One 6(6):e19831 |
| abstractText | The contribution of natural killer T (NKT) cells to the pathogenesis of metabolic abnormalities of obesity is controversial. While the combined genetic deletion of NKT and CD8(+) T-cells improves glucose tolerance and reduces inflammation, interpretation of these data have been complicated by the recent observation that the deletion of CD8(+) T-cells alone reduces obesity-induced inflammation and metabolic dysregulation, leaving the issue of the metabolic effects of NKT cell depletion unresolved. To address this question, CD1d null mice (CD1d(-)/(-)), which lack NKT cells but have a full complement of CD8(+) T-cells, and littermate wild type controls (WT) on a pure C57BL/6J background were exposed to a high fat diet, and glucose intolerance, insulin resistance, dyslipidemia, inflammation, and obesity were assessed. Food intake (15.5+/-4.3 vs 15.3+/-1.8 kcal/mouse/day), weight gain (21.8+/-1.8 vs 22.8+/-1.4 g) and fat mass (18.6+/-1.9 vs 19.5+/-2.1 g) were similar in CD1d(-)/(-) and WT, respectively. As would be expected from these data, metabolic rate (3.0+/-0.1 vs 2.9+/-0.2 ml O(2)/g/h) and activity (21.6+/-4.3 vs 18.5+/-2.6 beam breaks/min) were unchanged by NKT cell depletion. Furthermore, the degree of insulin resistance, glucose intolerance, liver steatosis, and adipose and liver inflammatory marker expression (TNFalpha, IL-6, IL-10, IFN-gamma, MCP-1, MIP1alpha) induced by high fat feeding in CD1d(-)/(-) were not different from WT. We conclude that deletion of NKT cells, in the absence of alterations in the CD8(+) T-cell population, is insufficient to protect against the development of the metabolic abnormalities of diet-induced obesity. |
