| First Author | Martin-Murphy BV | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 1 | Pages | e80949 |
| PubMed ID | 24465369 | Mgi Jnum | J:212306 |
| Mgi Id | MGI:5578450 | Doi | 10.1371/journal.pone.0080949 |
| Citation | Martin-Murphy BV, et al. (2014) Mice lacking natural killer T cells are more susceptible to metabolic alterations following high fat diet feeding. PLoS One 9(1):e80949 |
| abstractText | Current estimates suggest that over one-third of the adult population has metabolic syndrome and three-fourths of the obese population has non-alcoholic fatty liver disease (NAFLD). Inflammation in metabolic tissues has emerged as a universal feature of obesity and its co-morbidities, including NAFLD. Natural Killer T (NKT) cells are a subset of innate immune cells that abundantly reside within the liver and are readily activated by lipid antigens. There is general consensus that NKT cells are pivotal regulators of inflammation; however, disagreement exists as to whether NKT cells exert pathogenic or suppressive functions in obesity. Here we demonstrate that CD1d(-/-) mice, which lack NKT cells, were more susceptible to weight gain and fatty liver following high fat diet (HFD) feeding. Compared with their WT counterparts, CD1d(-/-) mice displayed increased adiposity and greater induction of inflammatory genes in the liver suggestive of the precursors of NAFLD. Calorimetry studies revealed a significant increase in food intake and trends toward decreased metabolic rate and activity in CD1d(-/-) mice compared with WT mice. Based on these findings, our results suggest that NKT cells play a regulatory role that helps to prevent diet-induced obesity and metabolic dysfunction and may play an important role in mechanisms governing cross-talk between metabolism and the immune system to regulate energy balance and liver health. |
