This review synthesizes human and animal data showing that pancreatic β-cell mass is largely set early in life, with proliferative capacity declining steeply after childhood and adult β-cells exhibiting long lifespans and limited ability to expand under metabolic stress. In both type 1 and type 2 diabetes, loss of functional β-cell mass reflects not only apoptosis but also dedifferentiation, where mature β-cells lose identity and revert toward progenitor-like states, reducing insulin output despite cell survival.
The authors discuss intrinsic brakes on β-cell proliferation, contested roles for neogenesis and transdifferentiation, emerging GLP‑1 receptor–based imaging methods to quantify β-cell mass, and therapeutic strategies—such as GLP‑1 receptor agonists and growth factor pathways—that may relieve ER/oxidative stress and preserve or restore functional β-cell mass. To learn more Click…
