Document Detail


Mutations in pancreatic ß-cell Glucokinase as a cause of hyperinsulinaemic hypoglycaemia and neonatal diabetes mellitus.
MedLine Citation:
PMID:  20878480     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Glucokinase is a key enzyme involved in regulating insulin secretion from the pancreatic ß-cell. The unique role of glucokinase in human glucose physiology is illustrated by the fact that genetic mutations in glucokinase can either cause hyperglycaemia or hypoglycaemia. Heterozygous inactivating mutations in glucokinase cause maturity-onset diabetes of the young (MODY), homozygous inactivating in glucokinase mutations result in permanent neonatal diabetes whereas heterozygous activating glucokinase mutations cause hyperinsulinaemic hypoglycaemia.
Authors:
Khalid Hussain
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Reviews in endocrine & metabolic disorders     Volume:  11     ISSN:  1573-2606     ISO Abbreviation:  Rev Endocr Metab Disord     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-11-08     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100940588     Medline TA:  Rev Endocr Metab Disord     Country:  United States    
Other Details:
Languages:  eng     Pagination:  179-83     Citation Subset:  IM    
Affiliation:
Clinical and Molecular Genetics Unit, The Developmental Endocrinology Research Group, Institute of Child Health, Hospital for Children NHS Trust, University College London, Great Ormond Street, London, UK. K.Hussain@ich.ucl.ac.uk
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Congenital hyperinsulinism and neonatal diabetes mellitus.
Next Document:  Role of 18F-DOPA PET/CT imaging in congenital hyperinsulinism.