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PMID: 11899241 Published · ppublish English Journal Article Review

The molecular basis of type 1 glycogen storage diseases.

Current molecular medicine ·Vol. 1 ·No. 1 ·2001-03-00 ·Pages 25-44

Chou JY

Abstract

Glycogen storage disease type 1 (GSD-1), also known as von Gierke disease, is a group of autosomal recessive metabolic disorders caused by deficiencies in the activity of the glucose-6-phosphatase (G6Pase) system that consists of at least two membrane proteins, glucose-6-phosphate transporter (G6PT) and G6Pase. G6PT translocates glucose-6-phosphate (G6P) from cytoplasm to the lumen of the endoplasmic reticulum (ER) and G6Pase catalyzes the hydrolysis of G6P to produce glucose and phosphate. Therefore, G6PT and G6Pase work in concert to maintain glucose homeostasis. Deficiencies in G6Pase and G6PT cause GSD-1a and GSD-1b, respectively. Both manifest functional G6Pase deficiency characterized by growth retardation, hypoglycemia, hepatomegaly, kidney enlargement, hyperlipidemia, hyperuricemia, and lactic acidemia. GSD-1b patients also suffer from chronic neutropenia and functional deficiencies of neutrophils and monocytes, resulting in recurrent bacterial infections as well as ulceration of the oral and intestinal mucosa. The G6Pase gene maps to chromosome 17q21 and encodes a 36-kDa glycoprotein that is anchored to the ER by 9 transmembrane helices with its active site facing the lumen. Animal models of GSD-1a have been developed and are being exploited to delineate the disease more precisely and to develop new therapies. The G6PT gene maps to chromosome 11q23 and encodes a 37-kDa protein that is anchored to the ER by 10 transmembrane helices. A functional assay for the recombinant G6PT protein has been established, which showed that G6PT functions as a G6P transporter in the absence of G6Pase. However, microsomal G6P uptake activity was markedly enhanced in the simultaneous presence of G6PT and G6Pase. The cloning of the G6PT gene now permits animal models of GSD-1b to be generated. These recent developments are increasing our understanding of the GSD-l disorders and the G6Pase system, knowledge that will facilitate the development of novel therapeutic approaches for these disorders.

MeSH Terms
Amino Acid Sequence Animals Binding Sites Disease Models, Animal Glucose-6-Phosphatase/chemistry,genetics,metabolism Glycogen Storage Disease Type I/enzymology,epidemiology,physiopathology,therapy Humans Mice Mice, Knockout Models, Biological Molecular Sequence Data Molecular Structure Mutation Neutropenia/physiopathology Protein Structure, Secondary Structure-Activity Relationship Tissue Distribution
Chemicals
Glucose-6-Phosphatase
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Chou J Y
Heritable Disorders Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. [email protected]
Article Info
Journal
Current molecular medicine
Abbr.
Curr Mol Med
ISSN
1566-5240
Published
2001-03-00
Pages
25-44
Language
English
Region
Netherlands
NLM ID
101093076
Subset
IM
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