Ion Channels and Transporters in Diabetes and Metabolic Diseases

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Background

Ion channels and transporters are key players in cell excitability, but they have also many other fundamental functions. For instance, they are crucial for chemical signalling (Ca2+ as a second messenger), transepithelial transport, regulation of cytoplasmic or vesicular ion concentration and pH, and regulation of cell volume. They are present not only in the plasma membrane but also in membranes of intracellular organelles such as the endoplasmic reticulum, endosomes, lysosomes and mitochondria.

Metabolic diseases are a worldwide epidemic, that have been linked to a broad spectrum of dysfunctional ion channels and transporters, which cause symptoms ranging from hypertension to endocrine disorders, kidney stones, and even dysmorphic features. The most notable metabolic disease is diabetes, resulting in impaired glucose homeostasis. The latter is a process of critical importance to human health as both hyper- and hypoglycaemia can lead to acute and long-term negative health outcomes.

The number of individuals with diabetes and metabolic diseases worldwide has risen exponentially over the last 40 years, therefore there is a pressing need to develop more effective therapies to improve patient outcome.

The goal of this topic collection is to discuss the new and old drug targets for the treatment of metabolic disorders mediated by the dysfunction of ion channels and transporters. For instance, in regard to diabetes glucose-regulatory hormone secretion, we are particularly interested in the role of pancreatic potassium (i.e. KATP, TALK-1), calcium and sodium channels alongside glucose (i.e. GLUT2) and lactate (i.e. MCT1) transporters. We are also interested to explore new therapeutic approach for obesity, involving the role of the TRPV1 channel via thermoregulation. Furthermore, changes in bone metabolism result from loss-of-function mutations in voltage-gated chloride channel (ClC-7) in bone metabolism, resulting in osteopetrosis. Mutations in KCNJ5, the gene that encodes an inwardly-rectifying potassium channel (Kir3.4) are associated with metabolic alkalosis in hyperaldosteronism.

As ion channels and transporters mediate different aspects of metabolism and glucose homeostasis, organ- and cell-type specific functions will be of particular interest, including but not limited to pancreatic hormone secretion, cardiac, kidney, and liver function.

We invite authors to contribute with Original Research Articles, Reviews and Mini Reviews focused on ion channels and transporters as a potential drug target for metabolic disorders. The themes covered by this collection include, but are not limited to, high quality research on:

• Physiological and pathophysiological mechanisms of islet hormone secretion
• Neonatal diabetes
• MODY
• Hyperinsulinemic hypoglycemia and different forms of diabetes mellitus
• Osteopetrosis as a result of dysfunctional channel
• Diabetic Kidney Disease (changes in renal ion channel activity)
• Thermogenesis as a new therapeutic approach for obesity
• Secondary complications of hyper/hypoglycaemia leading to changes in cardiac ion channel activity
• Role of mitochondrial ion channels and transporters in relation to diabetes and obesity

This project acknowledges the contribution of Dr. Thomas G Hill as an Editor Assistant.

Keywords: diabetes, voltage-gated channel, KATP, channelopathies, glucose disorders

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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