| First Author | Dror E | Year | 2017 |
| Journal | Nat Immunol | Volume | 18 |
| Issue | 3 | Pages | 283-292 |
| PubMed ID | 28092375 | Mgi Jnum | J:259365 |
| Mgi Id | MGI:6142286 | Doi | 10.1038/ni.3659 |
| Citation | Dror E, et al. (2017) Postprandial macrophage-derived IL-1beta stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nat Immunol 18(3):283-292 |
| abstractText | The deleterious effect of chronic activation of the IL-1beta system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1beta in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1beta, in a glucose-dependent manner. Subsequently, IL-1beta contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1beta signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1beta and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1beta mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium-glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1beta and insulin in the regulation of both metabolism and immunity. |
