| First Author | Bartolomé A | Year | 2022 |
| Journal | Diabetes | Volume | 71 |
| Issue | 11 | Pages | 2395-2401 |
| PubMed ID | 35944274 | Mgi Jnum | J:332851 |
| Mgi Id | MGI:7430646 | Doi | 10.2337/db22-0306 |
| Citation | Bartolome A, et al. (2022) An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak beta-Cell Mass Acquisition. Diabetes 71(11):2395-2401 |
| abstractText | The increase of functional beta-cell mass is paramount to maintaining glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow beta-cell mass adaptation may allow for the discovery of therapeutically actionable control nodes. In this study, we report the rapid and robust beta-cell hyperplasic effect in a mouse model of overfeeding-induced obesity (OIO) based on direct gastric caloric infusion. By performing RNA sequencing in islets isolated from OIO mice, we identified Sin3a as a novel transcriptional regulator of beta-cell mass adaptation. beta-Cell-specific Sin3a knockout animals showed profound diabetes due to defective acquisition of postnatal beta-cell mass. These findings reveal a novel regulatory pathway in beta-cell proliferation and validate OIO as a model for discovery of other mechanistic determinants of beta-cell adaptation. |
