Muscle Dysfunction Caused by a K ATP Channel Mutation in Neonatal Diabetes Is Neuronal in Origin
Copyright policy )Muscle Dysfunction Caused by a K ATP Channel Mutation in Neonatal Diabetes Is Neuronal in Origin
Brain Over Muscle Mutations in the gene encoding the Kir6.2 subunit of the adenosine triphosphate (ATP)–sensitive potassium (K ATP ) channel cause a specific type of neonatal diabetes in humans, known as iDEND, which is often accompanied by muscle weakness of unknown etiology. By studying mice expressing the mutant gene only in muscle or only in nerve, Clark et al. (p. 458 , published online 1 July) found that the motor impairments originate from inappropriate activation of the channel in the central nervous system rather than in muscle. Patients with iDEND are often treated with sulphonylurea therapies that block K ATP channels in both brain and muscle, and these drugs can have adverse effects on heart muscle. Drugs with greater specificity for K ATP channels in the brain may thus be a safer option.
- Churchill Hospital United Kingdom
- Oxford University Hospitals NHS Trust United Kingdom
- Oxford Centre for Diabetes, Endocrinology and Metabolism United Kingdom
- University of Oxford United Kingdom
- MRC Weatherall Institute of Molecular Medicine United Kingdom
Male, Neurons, Patch-Clamp Techniques, Muscles, Infant, Newborn, Mice, Transgenic, Motor Activity, Membrane Potentials, Mice, Adenosine Triphosphate, Gene Targeting, Diabetes Mellitus, Animals, Humans, Muscle Hypotonia, ATP-Binding Cassette Transporters, Ataxia, Female, Muscle Strength, Postural Balance
Male, Neurons, Patch-Clamp Techniques, Muscles, Infant, Newborn, Mice, Transgenic, Motor Activity, Membrane Potentials, Mice, Adenosine Triphosphate, Gene Targeting, Diabetes Mellitus, Animals, Humans, Muscle Hypotonia, ATP-Binding Cassette Transporters, Ataxia, Female, Muscle Strength, Postural Balance
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).94 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 1%
Citations provided by BIP!Popularity provided by BIP!