Glycogenosis Type III in the Dog

Čeh, L.; Jg, Hauge; Svenkerud, R; Strande, A

doi:10.1186/bf03547929

Cited by 28 publications

(1 citation statement)

References 13 publications

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“…In humans and other animals, high concentrations of glucose-6-phosphate and glycogen in skeletal muscle are associated with various forms of glycogenoses caused by deficiencies in glycogenolytic or glycolytic enzymes. 35,36 Glycolytic disorders can also develop in other species and include myophosphorylase deficiency in Charolais cattle, 37 acid maltase deficiency in Shorthorn cattle, 38 PFK deficiency in English Springer Spaniels, 39 debrancher deficiency in German Shepherd Dogs, 40 and glycogen branching-enzyme deficiency in QH foals. 41,42 Phosphofructokinase deficiency (glycogenosis type VII) is similar to PSSM in many respects; both disorders can result in the development of exertional rhabdomyolysis and accumulation of abnormal polysaccharides that are resistant to amylase digestion.…”

Section: Discussionmentioning

confidence: 99%

Insulin sensitivity in Belgian horses with polysaccharide storage myopathy

Firshman¹,

Valberg²,

Baird³

et al. 2008

ajvr

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Section: Discussionmentioning

confidence: 99%

Insulin sensitivity in Belgian horses with polysaccharide storage myopathy

Firshman¹,

Valberg²,

Baird³

et al. 2008

ajvr

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Models of Human Genetic Disease in Domestic Animals

Patterson

Haskins

Jezyk

1982

Advances in Human Genetics

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Glycogen storage diseases in animals and their potential value as models of human disease

Walvoort

1982

J of Inher Metab Disea

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Glycogen storage diseases (GSD) are inborn errors of glycogen metabolism. Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have been reported for GSD I (glucose-6-phosphatase deficiency) in the mouse, for GSD II (acid alpha-glucosidase 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-like conditions have been described in the rat (Acarbose-induced GSD II-like conditions, iodoacetate-induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A-induced symptoms of cyclic AMP-dependent 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.

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Glycogenosis Type III in the Dog

Cited by 28 publications

References 13 publications

Insulin sensitivity in Belgian horses with polysaccharide storage myopathy

Insulin sensitivity in Belgian horses with polysaccharide storage myopathy

Models of Human Genetic Disease in Domestic Animals

Glycogen storage diseases in animals and their potential value as models of human disease

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