| First Author | Liboz A | Year | 2025 |
| Journal | Cell Rep | Volume | 44 |
| Issue | 9 | Pages | 116283 |
| PubMed ID | 40946310 | Mgi Jnum | J:372458 |
| Mgi Id | MGI:8247821 | Doi | 10.1016/j.celrep.2025.116283 |
| Citation | Liboz A, et al. (2025) Beta-cell adaptation unveiled: The role of myokines in insulin-resistant mice. Cell Rep 44(9):116283 |
| abstractText | Pancreatic beta cells can adapt their mass and function to maintain normal glycemia when facing peripheral insulin resistance. To clarify the specific contribution and mechanisms of beta-cell mass adaptation in response to insulin resistance, we took advantage of genetic and pharmacologically induced insulin resistance in mice. We uncovered beta-cell expansion, via an increase in pancreatic islet density, as an adaptive mechanism triggered by mild-to-severe insulin resistance in young and older mice and documented pancreatic adaptation using 3D whole-pancreas analysis. Next, we found that insulin-resistant myotubes secrete factors that induce beta-cell differentiation. Using a combination of transcriptomic and functional analysis on a pancreatic differentiation model, we identified that myostatin, amphiregulin, and epiregulin can induce beta-cell differentiation in vitro. This work highlights how a physiological adaptation to insulin resistance can unlock the regenerative potential of myotube-derived peptides to trigger adaptive pancreatic beta-cell mass increase. |
