| First Author | Böni-Schnetzler M | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 11 | Pages | 103250 |
| PubMed ID | 34746709 | Mgi Jnum | J:313513 |
| Mgi Id | MGI:6798009 | Doi | 10.1016/j.isci.2021.103250 |
| Citation | Boni-Schnetzler M, et al. (2021) IL-1beta promotes the age-associated decline of beta cell function. iScience 24(11):103250 |
| abstractText | Aging is the prime risk factor for the development of type 2 diabetes. We investigated the role of the interleukin-1 (IL-1) system on insulin secretion in aged mice. During aging, expression of the protective IL-1 receptor antagonist decreased in islets, whereas IL-1beta gene expression increased specifically in the CD45 + islet immune cell fraction. One-year-old mice with a whole-body knockout of IL-1beta had higher insulin secretion in vivo and in isolated islets, along with enhanced proliferation marker Ki67 and elevated size and number of islets. Myeloid cell-specific IL-1beta knockout preserved glucose-stimulated insulin secretion during aging, whereas it declined in control mice. Isolated islets from aged myeloIL-1beta ko mice secreted more insulin along with increased expression of Ins2, Kir6.2, and of the cell-cycle gene E2f1. IL-1beta treatment of isolated islets reduced E2f1, Ins2, and Kir6.2 expression in beta cells. We conclude that IL-1beta contributes the age-associated decline of beta cell function. |
