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Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have been reported for GSD I (glucose\u20106\u2010phosphatase deficiency) in the mouse, for GSD II (acid \u03b1\u2010glucosidase deficiency) in the dog, in cattle and in the quail, for GSD III (debrancher enzyme deficiency) in the dog and for GSD VIII (phosphorylase kinase deficiency) in the rat and the mouse. Experimentally induced GSD\u2010like conditions have been described in the rat (Acarbose\u2010induced GSD II\u2010like conditions, iodoacetate\u2010induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A\u2010induced symptoms of cyclic AMP\u2010dependent protein kinase deficiency). Enzymatic defects that are typical of the human GSD types have not been clearly identified in the induced animal conditions. The homology of animal and human GSD types is discussed. It is concluded that clinical, pathogenic and therapeutic studies of GSD may benefit from the use of animal models. For genetic studies of human GSD these models may prove to be of limited value, as the picture of several human GSD types is already obscured by genetic heterogeneity.<\/jats:p>","DOI":"10.1007\/bf02391186","type":"journal-article","created":{"date-parts":[[2006,5,11]],"date-time":"2006-05-11T15:56:22Z","timestamp":1147362982000},"page":"3-16","source":"Crossref","is-referenced-by-count":32,"title":["Glycogen storage diseases in animals and their potential value as models of human disease"],"prefix":"10.1002","volume":"6","author":[{"given":"H. C.","family":"Walvoort","sequence":"first","affiliation":[{"name":"Laboratory for Pathology National Institute of Public Health  P. O. 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