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dc.contributor.authorDemirbilek, Huseyin
dc.contributor.authorGalcheva, Sonya
dc.contributor.authorVuralli, Dogus
dc.contributor.authorAl-Khawaga, Sara
dc.contributor.authorHussain, Khalid
dc.date.accessioned2021-06-02T10:39:49Z
dc.date.available2021-06-02T10:39:49Z
dc.date.issued2019
dc.identifier.issn1422-0067
dc.identifier.urihttp://dx.doi.org/10.3390/ijms20102590
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566632/
dc.identifier.urihttp://hdl.handle.net/11655/23822
dc.description.abstractIon 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.
dc.language.isoen
dc.relation.isversionof10.3390/ijms20102590
dc.rightsAttribution 4.0 United States
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleIon Transporters, Channelopathies, And Glucose Disorders
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalInternational Journal Of Molecular Sciences
dc.contributor.departmentÇocuk Sağlığı ve Hastalıkları
dc.identifier.volume20
dc.identifier.issue10
dc.description.indexPubMed
dc.description.indexWoS
dc.description.indexScopus


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Attribution 4.0 United States
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