Ions and Genes in Persistent Hyperinsulinaemic Hypoglycaemia in Infancy: A Commentary on the Implications for Tailoring Treatment to Disease Pathogenesis
- 1 January 1998
- journal article
- case report
- Published by Walter de Gruyter GmbH in Journal of Pediatric Endocrinology and Metabolism
- Vol. 11 (Supplement) , 121-130
- https://doi.org/10.1515/jpem.1998.11.s1.121
Abstract
No abstract availableThis publication has 22 references indexed in Scilit:
- Loss of functional KATP channels in pancreatic β–cells causes persistent hyperinsulinemic hypoglycemia of infancyNature Medicine, 1996
- Ionic control of beta cell function in nesidioblastosis. A possible therapeutic role for calcium channel blockade.Archives of Disease in Childhood, 1996
- Reconstitution of I KATP : An Inward Rectifier Subunit Plus the Sulfonylurea ReceptorScience, 1995
- The ABC of channel regulationCell, 1995
- Mutations in the Sulfonylurea Receptor Gene in Familial Persistent Hyperinsulinemic Hypoglycemia of InfancyScience, 1995
- Cloning of the β Cell High-Affinity Sulfonylurea Receptor: a Regulator of Insulin SecretionScience, 1995
- Potassium selective ion channels in insulin-secreting cells: physiology, pharmacology and their role in stimulus-secretion couplingBiochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, 1991
- Recent advances in hyperinsulinism and the pathogenesis of diabetes mellitusCurrent Opinion in Pediatrics, 1990
- Persistent Neonatal HyperinsulinismClinical Pediatrics, 1988
- Nesidioblastosis of the pancreas: definition of the syndrome and the management of the severe neonatal hyperinsulinaemic hypoglycaemia.Archives of Disease in Childhood, 1981