Blocking Ca2+ Channel β3 Subunit Reverses Diabetes

Abstract

Lee et al. report that pancreatic islets from diabetic mice overexpress Cavβ3, resulting in altered [Ca2+]i dynamics and impaired insulin secretion. Reducing Cavβ3 expression recovers islet dysfunction and glucose homeostasis. Experiments with human islets suggest that Cavβ3 may constitute a druggable target in diabetes treatment.