| First Author | Macdougall CE | Year | 2019 |
| Journal | Diabetes | Volume | 68 |
| Issue | 7 | Pages | 1473-1484 |
| PubMed ID | 31048369 | Mgi Jnum | J:276959 |
| Mgi Id | MGI:6315775 | Doi | 10.2337/db18-1243 |
| Citation | Macdougall CE, et al. (2019) Constitutive Activation of beta-Catenin in Conventional Dendritic Cells Increases the Insulin Reserve to Ameliorate the Development of Type 2 Diabetes in Mice. Diabetes 68(7):1473-1484 |
| abstractText | beta-Cell failure is central to the development of type 2 diabetes mellitus (T2DM). Dysregulation of metabolic and inflammatory processes during obesity contributes to the loss of islet function and impaired beta-cell insulin secretion. Modulating the immune system, therefore, has the potential to ameliorate diseases. We report that inducing sustained expression of beta-catenin in conventional dendritic cells (cDCs) provides a novel mechanism to enhance beta-cell insulin secretion. Intriguingly, cDCs with constitutively activated beta-catenin induced islet expansion by increasing beta-cell proliferation in a model of diet-induced obesity. We further found that inflammation in these islets was reduced. Combined, these effects improved beta-cell insulin secretion, suggesting a unique compensatory mechanism driven by cDCs to generate a greater insulin reserve in response to obesity-induced insulin resistance. Our findings highlight the potential of immune modulation to improve beta-cell mass and function in T2DM. |
