β-Cell dedifferentiation is a key mechanism of β-cell failure in type 2 diabetes (T2D). To survive metabolic stress, β-cells adopt a progenitor-like state, allowing for potential redifferentiation and T2D remission when conditions improve. Glucolipotoxicity is a known driver of β-cell failure, but the triggers of dedifferentiation remain unclear. Recent research has focused on pancreatic islet innervation, particularly the role of noradrenergic fibers in inhibiting insulin secretion. An increase in noradrenergic fibers has been correlated with β-cell dedifferentiation in humans, suggesting a role in T2D pathogenesis. This review explores the link between β-cell dedifferentiation and pancreatic noradrenergic innervation across murine and human models and examines the possibility of targeting innervation to reverse dedifferentiation, restore insulin secretion, and achieve T2D remission.
Avolio, A., Morciano, C., Gugliandolo, S., Splendore, A., Capece, U., Mezza, T., Di Giuseppe, G., Ciccarelli, G., Soldovieri, L., Brunetti, M., Pontecorvi, A., Giaccari, A., Cinti, F., The role of noradrenergic innervation and β-cell dedifferentiation in diabetes, <<TRENDS IN ENDOCRINOLOGY AND METABOLISM>>, 2026; (N/A): N/A-N/A. [doi:10.1016/j.tem.2026.04.005] [https://hdl.handle.net/10807/335597]
The role of noradrenergic innervation and β-cell dedifferentiation in diabetes
Avolio, Adriana;Morciano, Cassandra;Gugliandolo, Shawn;Splendore, Amelia;Capece, Umberto;Mezza, Teresa;Di Giuseppe, Gianfranco;Ciccarelli, Gea;Soldovieri, Laura;Brunetti, Michela;Pontecorvi, Alfredo;Giaccari, Andrea;Cinti, Francesca
Ultimo
2026
Abstract
β-Cell dedifferentiation is a key mechanism of β-cell failure in type 2 diabetes (T2D). To survive metabolic stress, β-cells adopt a progenitor-like state, allowing for potential redifferentiation and T2D remission when conditions improve. Glucolipotoxicity is a known driver of β-cell failure, but the triggers of dedifferentiation remain unclear. Recent research has focused on pancreatic islet innervation, particularly the role of noradrenergic fibers in inhibiting insulin secretion. An increase in noradrenergic fibers has been correlated with β-cell dedifferentiation in humans, suggesting a role in T2D pathogenesis. This review explores the link between β-cell dedifferentiation and pancreatic noradrenergic innervation across murine and human models and examines the possibility of targeting innervation to reverse dedifferentiation, restore insulin secretion, and achieve T2D remission.
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