Insulin secretion from pancreatic islet β-cells is governed by both metabolic and electrogenic pathways. The latter involves changes in membrane potential regulated by various potassium channels, including ATP-sensitive K + (K ATP ) channels, Ca 2+ -sensitive K + (K Ca ) channels, and voltage-dependent K + (Kv) channels. Glucose metabolism elevates the ATP/ADP ratio, leading to the closure of K ATP channels and subsequent membrane depolarization. Such depolarization opens voltage-dependent Ca 2+ channels (vDCCs), allowing Ca 2+ influx that triggers insulin release. The membrane is then repolarized through activation of K Ca and Kv channels. Multiple K Ca and Kv channel subtypes have been identified in insulin-secreting cells, with emerging evidence highlighting their significant modulatory roles in glucose-stimulated insulin secretion (GSIS). In this review, the current understanding and therapeutic potential of Kv channels in insulin secretion are discussed in relation to the structural features and physiological functions.
Xing et al. (Mon,) studied this question.