ReviewHuman genetics2005
Current status of the E23K Kir6.2 polymorphism: implications for type-2 diabetes.
Review in Human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Evidence for association of the E23K variant of KCNJ11 gene with type 2 diabetes in Tunisian population: population-based study and meta-analysis.BioMed research international · 2014Pooled it
- Validation of Genome-Wide Association Studies (GWAS)-Identified Type 2 Diabetes Mellitus Risk Variants in Pakistani Pashtun Population.Journal of the ASEAN Federation of Endocrine Societies · 2023Article
- ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?Diabetes · 2022Review
- Ischemic Heart Disease and Heart Failure: Role of Coronary Ion Channels.International journal of molecular sciences · 2020Review
- Contribution of systemic inflammation to permanence of KAmerican journal of physiology. Endocrinology and metabolism · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Pharmacogenetics of posttransplant diabetes mellitus.The pharmacogenomics journal · 2017Review
- Expression and function of ATP-dependent potassium channels in zebrafish islet β-cells.Royal Society open science · 2017Article
- Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk.Diabetologia · 2016Article
- Modeling K,ATP--dependent excitability in pancreatic islets.Biophysical journal · 2014Article
- Pancreatic β cell dedifferentiation in diabetes and redifferentiation following insulin therapy.Cell metabolism · 2014Article
- Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease.Basic research in cardiology · 2013Observational
- Channeling dysglycemia: ion-channel variations perturbing glucose homeostasis.Trends in endocrinology and metabolism: TEM · 2012Review
- The ATP-sensitive K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase activity.Diabetes · 2012Article
- The interactive effect of SIRT1 promoter region polymorphism on type 2 diabetes susceptibility in the North Indian population.PloS one · 2012Article
- The molecular genetics of sulfonylurea receptors in the pathogenesis and treatment of insulin secretory disorders and type 2 diabetes.Current diabetes reports · 2011Review
- Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.Diabetes · 2011Article
- Current understanding of K ATP channels in neonatal diseases: focus on insulin secretion disorders.Acta pharmacologica Sinica · 2011Review
- K(ATP) channelopathies in the pancreas.Pflugers Archiv : European journal of physiology · 2010Review
- Human K(ATP) channelopathies: diseases of metabolic homeostasis.Pflugers Archiv : European journal of physiology · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ATP-sensitive potassium (KATP) channel couples membrane excitability to cellular metabolism and is a critical mediator in the process of glucose-stimulated insulin secretion. Increasing numbers of KATP channel polymorphisms are being described and linked to altered insulin secretion indicating that genes encoding this ion channel could be susceptibility markers for type-2 diabetes. Genetic variation of KATP channels may result in altered beta-cell electrical activity, glucose homeostasis, and increased susceptibility to type-2 diabetes. Of particular interest is the Kir6.2 E23K polymorphism, which is linked to increased susceptibility to type-2 diabetes in Caucasian populations and may also be associated with weight gain and obesity, both of which are major diabetes risk factors. This association highlights the potential contribution of both genetic and environmental factors to the development and progression of type-2 diabetes. In addition, the common occurrence of the E23K polymorphism in Caucasian populations may have conferred an evolutionary advantage to our ancestors. This review will summarize the current status of the association of KATP channel polymorphisms with type-2 diabetes, focusing on the possible mechanisms by which these polymorphisms alter glucose homeostasis and offering insights into possible evolutionary pressures that may have contributed to the high prevalence of KATP channel polymorphisms in the Caucasian population.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.