Glucose and NAADP trigger elementary intracellular β-cell Ca²⁺ signals.

ABSTRACT: Pancreatic β-cells release insulin upon a rise in blood glucose. The precise mechanisms of stimulus-secretion coupling, and its failure in Diabetes Mellitus Type 2, remain to be elucidated. The consensus model, as well as a class of currently prescribed anti-diabetic drugs, are based around the observation that glucose-evoked ATP production in β-cells leads to closure of cell membrane ATP-gated potassium (K_ATP) channels, plasma membrane depolarisation, Ca²⁺ influx, and finally the exocytosis of insulin granules. However, it has been demonstrated by the inactivation of this pathway using genetic and pharmacological means that closure of the K_ATP channel alone may not be sufficient to explain all β-cell responses to glucose elevation. We have previously propo

SUBMITTER: Heister PM 

PROVIDER: S-EPMC8140081 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature