منابع مشابه
KATP Channel Mutations and Neonatal Diabetes
Since the discovery of the KATP channel in 1983, numerous studies have revealed its physiological functions. The KATP channel is expressed in various organs, including the pancreas, brain and skeletal muscles. It functions as a "metabolic sensor" that converts the metabolic status to electrical activity. In pancreatic beta-cells, the KATP channel regulates the secretion of insulin by sensing a ...
متن کاملNeonatal Diabetes and the KATP Channel: From Mutation to Therapy
Activating mutations in one of the two subunits of the ATP-sensitive potassium (KATP) channel cause neonatal diabetes (ND). This may be either transient or permanent and, in approximately 20% of patients, is associated with neurodevelopmental delay. In most patients, switching from insulin to oral sulfonylurea therapy improves glycemic control and ameliorates some of the neurological disabiliti...
متن کاملSulfonylurea for the treatment of neonatal diabetes owing to KATP-channel mutations: a systematic review and meta-analysis
The effect of sulfonylurea for the treatment of neonatal diabetes (NDM) is remain uncertain. We conducted this systematic review and meta-analysis to investigate the effect of sulfonylurea for NDM and to provide the latest and most convincing evidence for developing clinical practice guidelines of NDM. A literature review was performed to identify all published studies reporting the sulfonylure...
متن کاملPerspectives in Diabetes Diabetes and Insulin Secretion The ATP-Sensitive K Channel (KATP) Connection
The ATP-sensitive K channel (KATP channel) senses metabolic changes in the pancreatic -cell, thereby coupling metabolism to electrical activity and ultimately to insulin secretion. When KATP channels open, -cells hyperpolarize and insulin secretion is suppressed. The prediction that KATP channel “overactivity” should cause a diabetic state due to undersecretion of insulin has been dramatically ...
متن کاملLeptin-stimulated KATP channel trafficking
Insulin secretion from pancreatic β-cells is initiated by the closure of ATP-sensitive K+ channels (KATP) in response to high concentrations of glucose, and this action of glucose is counteracted by the hormone leptin, an adipokine that signals through the Ob-Rb receptor to increase KATP channel activity. Despite intensive investigations, the molecular basis for KATP channel regulation remains ...
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ژورنال
عنوان ژورنال: Endocrine Journal
سال: 2009
ISSN: 0918-8959,1348-4540
DOI: 10.1507/endocrj.k08e-160