title: Metabolic syndrome and ionic channels in pancreatic beta cells.
abstract: Worldwide increase in the prevalence of metabolic syndrome and diabetes mellitus type 2 (DM2) during the past decades has converted them into a global epidemic disease. It is not well understood how these metabolic disorders initiate, but an increase in food consumption associated to low physical activity leads to increase in body weight and obesity. This in turn, elevates circulating lipids and cytokines release by adipose tissue, give the organism a chronic inflammation and potentiate insulin secretion, causing insulin resistance. Depending on genetics and probably other environmental factors, after a long period of hyperactivity, pancreatic beta cells become exhausted and DM2 overcomes. Pancreatic beta cells are the only source of insulin known in mammals. They are unique because of their ability to sense and transform fuels into a chemical signal, which affects mainly all the cells in the organism. Many other factors affect insulin secretion. We will focus on the alterations of glucose-induced insulin secretion coupling, particularly in ionic channels that have crucial importance in this process. Different channel types can be affected by metabolic syndrome. The most studied are K(ATP) and other potassium channels, calcium, sodium, and TRP channels. Much information comes from rodents that do not express exactly the same proportion and type of channels than humans. However, getting insight of how do they participate in insulin secretion and how to modulate them is important to completely understand beta-cell physiology and pathophysiological reactions to metabolic syndrome and diabetes, in order to stop the epidemic of these metabolic disorders.
authors.affiliation: Department of Neural Development and Physiology, Neuroscience Division, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico, Mexico. Electronic address: mhiriart@ifc.unam.mx.
authors.forename: Marcia
authors.initials: M
authors.lastname: Hiriart
authors.affiliation: Department of Neural Development and Physiology, Neuroscience Division, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico, Mexico.
authors.forename: Myrian
authors.initials: M
authors.lastname: Velasco
authors.affiliation: Department of Neural Development and Physiology, Neuroscience Division, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico, Mexico.
authors.forename: Carlos
authors.initials: C
authors.lastname: Larqué
authors.affiliation: Department of Neural Development and Physiology, Neuroscience Division, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico, Mexico.
authors.forename: Carlos Manlio
authors.initials: CM
authors.lastname: Diaz-Garcia
mesh_terms: D000818:Animals; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000473:pathology; D007473:Ion Channels / Q000378:metabolism*; D024821:Metabolic Syndrome / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D010179:Pancreas / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D007328:Insulin; D007473:Ion Channels
keywords: Calcium channels; GLUT2; Insulin receptor; Insulin secretion; Potassium channels; Sodium channels; Type 2 diabetes