Glucose-stimulated pancreatic islets show α cell mass dependent fast and slow Ca2+ oscillations. It implicates structure-function relationship is a fundamental principle of pancreatic islets. Despite the low percentage within the islet, the δ cells entangle with α cells and occupy the islet periphery, to envelop the β cells in the core. However, the contribution of the extensive δ-α paracrine organization to the origin of the variability in Ca2+ activation, remains unclear. Here we found that somatostatin’s perturbation on Ca2+ oscillation critically depended on α cell mass. Furthermore, pharmacological and opto-geneticalperturbation on δ-α cell interaction cause islets to repeatably show fast and slow Ca2+ oscillations. Our study highlights the importance of δ-α cell interactions as the origin of the variability in oscillation pattern. Studying islets in their intact pancreas morphology in tissue slice revealed that glucose recruited the δ cells to control the α and β cell activity.
H.Ren: None.
