Background and Purpose: Quercetin is a natural polyphenolic flavonoid that displays anti‐diabetic properties in vivo. Its mechanism of action on insulin‐secreting beta cells is poorly documented. In this work, we have analysed the effects of quercetin both on insulin secretion and on the intracellular calcium concentration ([Ca2+]i) in beta cells, in the absence of any co‐stimulating factor.Experimental Approach: Experiments were performed on both INS‐1 cell line and rat isolated pancreatic islets. Insulin release was quantified by the homogeneous time‐resolved fluorescence method. Variations in [Ca2+]i were measured using the ratiometric fluorescent Ca2+ indicator Fura‐2. Ca2+ channel currents were recorded with the whole‐cell patch‐clamp technique.Key Results: Quercetin concentration‐dependently increased insulin secretion and elevated [Ca2+]i. These effects were not modified by the SERCA inhibitor thapsigargin (1 μmol·L−1), but were nearly abolished by the L‐type Ca2+ channel antagonist nifedipine (1 μmol·L−1). Similar to the L‐type Ca2+ channel agonist Bay K 8644, quercetin enhanced the L‐type Ca2+ current by shifting its voltage‐dependent activation towards negative potentials, leading to the increase in [Ca2+]i and insulin secretion. The effects of quercetin were not inhibited in the presence of a maximally active concentration of Bay K 8644 (1 μmol·L−1), with the two drugs having cumulative effects on [Ca2+]i.Conclusions and Implications: Taken together, our results show that quercetin stimulates insulin secretion by increasing Ca2+ influx through an interaction with L‐type Ca2+ channels at a site different from that of Bay K 8644. These data contribute to a better understanding of quercetin's mechanism of action on insulin secretion.