Abstract
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. Voltage-dependent Ca2+ channel 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 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 type 2 diabetes.
Original language | English (US) |
---|---|
Pages (from-to) | 1326-1346 |
Number of pages | 21 |
Journal | Journal of molecular biology |
Volume | 432 |
Issue number | 5 |
DOIs | |
State | Published - Mar 6 2020 |
Keywords
- calcium
- glucagon
- glucose
- insulin
- β-cells
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Molecular Biology