Abstract
Ion channels and transporters play essential roles in excitable cells including cardiac, skeletal and smooth muscle cells, neurons, and endocrine cells. In pancreatic beta-cells, for example, potassium KATP channels link the metabolic signals generated inside the cell to changes in the beta-cell membrane potential, and ultimately regulate insulin secretion. Mutations in the genes encoding some ion transporter and channel proteins lead to disorders of glucose homeostasis (hyperinsulinaemic hypoglycaemia and different forms of diabetes mellitus). Pancreatic KATP, Non-KATP, and some calcium channelopathies and MCT1 transporter defects can lead to various forms of hyperinsulinaemic hypoglycaemia (HH). Mutations in the genes encoding the pancreatic KATP channels can also lead to different types of diabetes (including neonatal diabetes mellitus (NDM) and Maturity Onset Diabetes of the Young, MODY), and defects in the solute carrier family 2 member 2 (SLC2A2) leads to diabetes mellitus as part of the Fanconi–Bickel syndrome. Variants or polymorphisms in some ion channel genes and transporters have been reported in association with type 2 diabetes mellitus.
Highlights
Ion channels and transporters are membrane-embedded proteins which play a key role in transporting ions and biomolecules across cell membranes
We focus on ion channel and transporter function in relation to glucose physiology
Maturity-onset diabetes of the young (MODY) is a group of non-autoimmune diabetes caused by a single gene mutation that leads to a defect in the glucose-stimulated insulin secretion from the pancreatic beta-cells
Summary
Ion channels and transporters are membrane-embedded proteins which play a key role in transporting ions and biomolecules across cell membranes. The flow of ions across the channel (transmembrane flux) creates an electrical signal or action potential which is essential for the function of the particular channel [1]. Another property of ion channels is gating, which allows the channels to open and close in response to certain specific stimuli. We will firstly describe the role of ion channels and transporters in relation to insulin secretion from the pancreatic beta-cell and describe mechanistic insights into how defects in ion channels and transporters lead to hyperinsulinaemic hypoglycemia and diabetes mellitus
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