Role of Ion Channel Modulator in Diabetes Mellitus
Poonam Singh, Vaibhav Walia and Prabhakar Kumar Verma*
Department of Pharmaceutical Sciences, Maharshi Dayanand University, Rohtak, Haryana, India
*Corresponding Author: Prabhakar Kumar Verma, Department of Pharmaceutical Sciences, Maharshi Dayanand University, Rohtak, Haryana, India.
November 01, 2021; Published: December 16, 2021
Ion channel playa essential role in glucose induced insulin secretion. Insulin secretion by β cells of pancreas that response to an increase the blood glucose levels in body. It plays an important role to maintain homeostasis of glucose. Glucose stimulated insulin secretion (GSIS) in β cells of pancreas have explored. Glucose enters in cell membrane then later in metabolic pathway. In this manner the ratio of ATP/ADP (adenosine triphosphate/adenosine di-phosphate) increase cause to closing of ATP-sensitive potassium channel (KATP) channels leading to depolarization of membrane. Depolarization cause to opening of voltage gated sodium channels (Nav) later voltage dependent calcium channels (Cav). Increasing of calcium in intra-cellular membrane cause the insulin exocytosis from insulin containing vesicles. Then electrical activity of β cell of pancreas plays an important role in the GSIS. Furthermore, incretins, some neurotransmitters hormones and growth factors, can modulate the GSIS. In this review we discuss on ion channels and types of ion channel, role of KATP, Nav, Cav and Cl channels in insulin secretion, expression of ion channel, alteration of ion channel in diabetes mellitus disorder, ion channel as a drug target in diabetes mellitus.
Keywords: Ion Channel; Diabetes Mellitus; Insulin Secretion; Pancreatic Β Cell
- Hille B. “Ion channels of excitable membranes. Sinauer Associates”. Sunderland, MA (2001): 814.
- Gabashvili A., et al. “Templating mesoporous silica with chiral block copolymers and its application for enantioselective separation”. The Journal of Physical Chemistry B38 (2007): 11105-10.
- Doyle DA., et al. “The structure of the potassium channel: molecular basis of K+ conduction and selectivity”. Science5360 (1998): 69-77.
- Dutzler R., et al. “X-ray structure of a ClC chloride channel at 3.0 Å reveals the molecular basis of anion selectivity”. Nature6869 (2002): 287-294.
- Payandeh J., et al. “The crystal structure of a voltage-gated sodium channel”. Nature7356 (2011): 353-358.
- Overington JP., et al. “How many drug targets are there?”. Nature reviews Drug discovery12 (2006): 993-996.
- Anger T., et al. “Medicinal chemistry of neuronal voltage-gated sodium channel blockers”. Journal of medicinal chemistry2 (2001): 115-137.
- Proks P and Lippiat JD. “Membrane ion channels and diabetes”. Current pharmaceutical design4 (2006): 485-501
- Parrott A., et al. “Role of rural land use management in flood and coastal risk management”. Journal of Flood Risk Management4 (2009): 272-284.
- Armstrong CM and Bezanilla F. “Charge movement associated with the opening and closing of the activation gates of the Na channels”. The Journal of general physiology5 (1974): 533-552.
- Long SB., et al. “Crystal structure of a mammalian voltage-dependent Shaker family K+ channel”. Science5736 (2005): 897-903.
- Ertel EA., et al. “Nomenclature of voltage-gated calcium channels”. Neuron 25.3 (2000): 533-535.
- Catterall WA., et al. “International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels”. Pharmacological reviews 57.4 (2005): 397-409.
- Nelson M. “Drug treatment of elevated blood pressure”. Australian Prescriber 33.4 (2010): 108-112.
- Ashcroft FM and Rorsman P. “Electrophysiology of the pancreatic β-cell”. Progress in biophysics and molecular biology2 (1989): 87-143.
- Hiriart M and Aguilar-Bryan L. “Channel regulation of glucose sensing in the pancreatic β-cell”. American Journal of Physiology-Endocrinology and Metabolism 295.6 (2008): E1298-1306.
- Kitaguchi T., et al. “Extracellular calcium influx activates adenylate cyclase 1 and potentiates insulin secretion in MIN6 cells”. Biochemical Journal2 (2013): 365-373.
- Davalli AM., et al. “Dihydropyridine-sensitive and-insensitive voltage-operated calcium channels participate in the control of glucose-induced insulin release from human pancreatic β cells”. Journal of Endocrinology2 (1996): 195-203.
- Schmutz J., et al. “Genome sequence of the palaeopolyploid soybean”. nature7278 (2010): 178-183.
- Iwashima Y., et al. “Expression of calcium channel mRNAs in rat pancreatic islets and downregulation after glucose infusion”. Diabetes7 (1993): 948-955.
- Scholze A., et al. “Functional expression and characterization of a voltage-gated CaV1. 3 (α1D) calcium channel subunit from an insulin-secreting cell line”. Molecular Endocrinology7 (2001): 1211-1221.
- Rorsman P., et al. “Regulation of calcium in pancreatic α-and β-cells in health and disease”. Cell calcium3-4 (2012): 300-308.
- Hiriart M and Matteson DR. “Na channels and two types of Ca channels in rat pancreatic B cells identified with the reverse hemolytic plaque assay”. The Journal of general physiology5 (1988): 617-639.
- Roe MW., et al. “NIDDM is associated with loss of pancreatic beta-cell L-type Ca2+ channel activity”. American Journal of Physiology-Endocrinology and Metabolism1 (1996): E133-140.
- Kato S., et al. “Increased calcium-channel currents of pancreatic β cells in neonatally streptozocin-induced diabetic rats”. Metabolism11 (1994): 1395-1400.
- Thomas Jessell., et al. Principles of neural science (2000).
- Braun M., et al. “Voltage-gated ion channels in human pancreatic β-cells: electrophysiological characterization and role in insulin secretion”. Diabetes6 (2008): 1618-1628.
- Vignali S., et al. “Characterization of voltage‐dependent sodium and calcium channels in mouse pancreatic A‐and B‐cells”. The Journal of physiology3 (2006): 691-706.
- Suckale J and Solimena M. “The insulin secretory granule as a signaling hub”. Trends in Endocrinology & Metabolism10 (2010): 599-609.
- Satin LS., et al. “Inactivation of HIT cell Ca2+ current by a simulated burst of Ca2+ action potentials”. Biophysical journal1 (1994): 141-148.
- Hong S and Wiley JW. “Altered expression and function of sodium channels in large DRG neurons and myelinated A-fibers in early diabetic neuropathy in the rat”. Biochemical and biophysical research communications2 (2006): 652-660.
- Trujillo TC and Nolan PE. “Antiarrhythmic agents”. Drug safety 23.6 (2000): 509-32.
- Drews G., et al. “Electrophysiology of islet cells”. Advances in Experimental Medicine and Biology (2010): 115-163.
- Renström E., et al. “Sulfonylurea-mediated stimulation of insulin exocytosis via an ATP-sensitive K+ channel–independent action”. Diabetes1 (2002): S33-S36.
- Tabcharani JA and Misler S. “Ca2+-activated K+ channel in rat pancreatic islet B cells: permeation, gating and blockade by cations”. Biochimica et Biophysica Acta (BBA)-Biomembranes1(1989): 62-72.
- Henquin JC. “Role of voltage-and Ca 2+-dependent K+ channels in the control of glucose-induced electrical activity in pancreatic B-cells”. PflügersArchiv5 (1990): 568-572.
- Philipson LH., et al. “Sequence and functional expression in Xenopus oocytes of a human insulinoma and islet potassium channel”. Proceedings of the National Academy of Sciences1 (1991): 53-7.
- Koster JC., et al. “Targeted overactivity of β cell KATP channels induces profound neonatal diabetes”. Cell6 (2000): 645-654.
- Sakura H., et al. “Glucose modulation of ATP-sensitive K-currents in wild-type, homozygous and heterozygous glucokinase knock-out mice”. Diabetologia6 (1998): 654-659.
- Ashcroft SJ and Ashcroft FM. “Properties and functions of ATP-sensitive K-channels”. Cellular signalling 3 (1990): 197-214.
- Rorsman P., et al. “Regulation of calcium in pancreatic α-and β-cells in health and disease”. Cell calcium 51.3-4 (2012): 300-308.
- Namkung W., et al. “Inhibition of Ca2+-activated Cl− channels by gallotannins as a possible molecular basis for health benefits of red wine and green tea”. The FASEB Journal11 (2010): 4178-4186.
- Iden S., et al. “A distinct PAR complex associates physically with VE‐cadherin in vertebrate endothelial cells”. EMBO reports12 (2006): 1239-1246.
- Campbell JD., et al. “Potassium channel regulation”. EMBO reports11 (2003): 1038-1042.
- Jing X., et al. “Ca V 2.3 calcium channels control second-phase insulin release”. The Journsal of clinical investigation1 (2005): 146-154.
- Ämmälä C., et al. “Calcium-independent potentiation of insulin release by cyclic AMP in single β-cells”. Nature6427 (1993): 356-358.
- Ammälä C., et al. “Activation of protein kinases and inhibition of protein phosphatases play a central role in the regulation of exocytosis in mouse pancreatic beta cells”. Proceedings of the National Academy of Sciences10 (1994): 4343-4347.
- Renström E., et al. “Neurotransmitter-induced inhibition of exocytosis in insulin-secreting β cells by activation of calcineurin”. Neuron3 (1996): 513-522.
- Black JA., et al. “Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain”. Pain3 (2004): 237-247.