LAUSR

Ca2+ is an essential signal for pancreatic β-cell function. Ca2+ plays critical roles in numerous β-cell pathways such as insulin secretion, transcription, metabolism, endoplasmic reticulum function and the stress response. Therefore, β-cell Ca2+ handling is tightly controlled. At the plasma membrane Ca2+ entry primarily occurs through voltage-dependent Ca2+ channels (VDCCs). VDCC activity is dependent on orchestrated fluctuations in the plasma membrane potential or voltage, which are mediated via the activity of many ion channels. During the pathogenesis of type-2 diabetes (T2D) the β-cell is exposed to stressful conditions, which result in alterations of Ca2+ handling. Some of the changes in β-cell Ca2+ handling that occur under stress result from perturbations in ion channel activity, expression or localization. Defective Ca2+ signaling in the diabetic β-cell alters function, limits insulin secretion and exacerbates hyperglycemia. In this review, we focus on the β-cell ion channels that control Ca2+ handling and how they impact β-cell dysfunction in T2D.