| Literature DB >> 31473158 |
David A Jacobson1, Show-Ling Shyng2.
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.Entities:
Keywords: calcium; glucagon; glucose; insulin; β-cells
Mesh:
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Year: 2019 PMID: 31473158 PMCID: PMC7720859 DOI: 10.1016/j.jmb.2019.08.014
Source DB: PubMed Journal: J Mol Biol ISSN: 0022-2836 Impact factor: 5.469