Glucose-stimulated pancreatic islets show different patterns of Ca2+ signaling with fast, slow and mixed fast/slow oscillations. However, it is not clear whether they are characteristic features of individual islets. We report islet spontaneous slowdown from fast to slow/mixed Ca2+ oscillation under high glucose stimulation. The fast oscillation stage typically lasts for several hours and intrinsic to the islet. The modes switch is reversible. Low glucose resting for 30 minutes fully restored the fast oscillation. Microfluidic perfusion delays and static incubation brings forward the mode switch, which suggests the critical role of the paracrine environment. Correspondingly, exogenous glucagon delays and somatostatin brings forward the mode switch. Pharmacologically blocking Sstr2 on α cells triggers endogenous glucagon secretion and switches islets back to fast oscillations. Optoinhibition and relief of δ cells cause islets to repeatably show fast and slow oscillations. Our study highlights the importance of δ-α cell interactions to generate tunable islet oscillation patterns. The design principle of pancreatic islet was revealed, as the minority of δ cells command the majority of α and β cells.