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Ca 2+ handling by the endoplasmic reticulum (ER) serves critical roles in controlling pancreatic β cell function and becomes perturbed during the pathogenesis of diabetes. ER Ca 2+ homeostasis is determined by ion movements across the ER membrane, including K + flux through K + channels. We demonstrated that K + flux through ER-localized TALK-1 channels facilitated Ca 2+ release from the ER in mouse and human β cells. We found that β cells from mice lacking TALK-1 exhibited reduced basal cytosolic Ca 2+ and increased ER Ca 2+ concentrations, suggesting reduced ER Ca 2+ leak. These changes in Ca 2+ homeostasis were presumably due to TALK-1-mediated ER K + flux, because we recorded K + currents mediated by functional TALK-1 channels on the nuclear membrane, which is continuous with the ER. Moreover, overexpression of K + -impermeable TALK-1 channels in HEK293 cells did not reduce ER Ca 2+ stores. Reduced ER Ca 2+ content in β cells is associated with ER stress and islet dysfunction in diabetes, and islets from TALK-1-deficient mice fed a high-fat diet showed reduced signs of ER stress, suggesting that TALK-1 activity exacerbated ER stress. Our data establish TALK-1 channels as key regulators of β cell ER Ca 2+ and suggest that TALK-1 may be a therapeutic target to reduce ER Ca 2+ handling defects in β cells during the pathogenesis of diabetes.

TALK-1 channels control β cell endoplasmic reticulum Ca 2+ homeostasis

TALK-1 channels control β cell endoplasmic reticulum Ca ²⁺ homeostasis