Fig. 3.

Schematic depicting primary cilia regulation of hormone secretion and islet cell crosstalk. Genetic deletion of β-cell cilia leads to reduced glucose-stimulated insulin secretion via suggested mechanisms depicted in the box. β-Cell inhibition by δ-cell-derived somatostatin is also blocked in the β-cell specific cilia knockout (βCKO) model, suggesting that primary cilia on β-cells mediates paracrine somatostatin signaling. Meanwhile, β-cell response to glucagon appears to remain intact in βCKO islets, suggesting that some but not all paracrine signals are regulated by the β-cell primary cilium. EphA, epoxide hydrolase A; GPCR, G-protein coupled receptor.