| First Author | Kimura H | Year | 2016 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 311 |
| Issue | 5 | Pages | E881-E890 |
| PubMed ID | 27702746 | Mgi Jnum | J:241395 |
| Mgi Id | MGI:5901992 | Doi | 10.1152/ajpendo.00174.2016 |
| Citation | Kimura H, et al. (2016) Caspase-1 deficiency promotes high-fat diet-induced adipose tissue inflammation and the development of obesity. Am J Physiol Endocrinol Metab 311(5):E881-E890 |
| abstractText | Caspase-1 is a cysteine protease responsible for the processing of the proinflammatory cytokine interleukin-1beta and activated by the formation of inflammasome complexes. Although several investigations have found a link between diet-induced obesity and caspase-1, the relationship remains controversial. Here, we found that mice deficient in caspase-1 were susceptible to high-fat diet-induced obesity with increased adiposity as well as normal lipid and glucose metabolism. Caspase-1 deficiency clearly promoted the infiltration of inflammatory macrophages and increased the production of C-C motif chemokine ligand 2 (CCL2) in the adipose tissue. The dominant cellular source of CCL2 was stromal vascular fraction rather than adipocytes in the adipose tissue. These findings demonstrate a critical role of caspase-1 in macrophage-driven inflammation in the adipose tissue and the development of obesity. These data provide novel insights into the mechanisms underlying inflammation in the pathophysiology of obesity. |
