Neonatal diabetes and the KATP channel: from mutation to therapy
FM Ashcroft, MC Puljung, N Vedovato - Trends in Endocrinology & …, 2017 - cell.com
FM Ashcroft, MC Puljung, N Vedovato
Trends in Endocrinology & Metabolism, 2017•cell.comActivating mutations in one of the two subunits of the ATP-sensitive potassium (K ATP)
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 disabilities. Here, we review how K ATP channel
mutations lead to the varied clinical phenotype, how sulfonylureas exert their therapeutic …
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 disabilities. Here, we review how K ATP channel
mutations lead to the varied clinical phenotype, how sulfonylureas exert their therapeutic …
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 disabilities. Here, we review how KATP channel mutations lead to the varied clinical phenotype, how sulfonylureas exert their therapeutic effects, and why their efficacy varies with individual mutations.
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