Somatostatin triggers local cAMP and Ca2+ signaling in primary cilia to modulate pancreatic β-cell function

ABSTRACT: Somatostatin, released from δ-cells within pancreatic islets of Langerhans, is one of the most important negative regulators of islet hormone secretion. We find that islet δ-cells are positioned near, and release somatostatin onto, primary cilia of the other islet cell types, including insulin-secreting β-cells. Somatostatin activates ciliary somatostatin receptors, resulting in rapid lowering of the ciliary cAMP concentration which in turn promotes more sustained nuclear translocation of the cilia-dependent transcription factor GLI2 through a mechanism that operates in parallel with the canonical Hedgehog pathway and depends on ciliary Ca2+ signaling. We also find that primary cilia length is reduced in islets from human donors with type-2 diabetes, which is associated with a reduction in

SUBMITTER: Tugce, Ceren Incedal 

PROVIDER: S-SCDT-10_1038-S44318-025-00383-7 | biostudies-other |

REPOSITORIES: biostudies-other