Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver glucose-6-phosphatase and lipase-esterase, liver and muscle glycogen phosphorylase, and brown fat lipase-esterase activity changes were studied during the postnatal development of rats born and growing up in temperatures of +5 and 20 degrees C. Liver glucose-6-phosphatase activity was highest at the age of 4 days in both environments. In the age groups 20-67 days glucose-6-phosphatase activity was higher in animals living in a cold environment than in those reared at room temperature. At birth, glycogen phosphorylase activity was high in the liver but very low in the muscle. No difference was found between the two temperatures. The lipase-esterase activity in the liver was very low at birth, rising to adult level by the age of 30 days, while in the brown fat the activity was already high at the time of birth and clearly higher in rats born in a cold environment than in those born at room temperature. At the time of birth the relative and absolute weight of brown fat were also clearly higher in rats born at +5 degrees C than in those born +20 degrees C.
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PMID:Effects of a cold environment on energy-related enzyme activities in the postnatal rat. 17 36

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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PMID:Glycogen storage diseases in animals and their potential value as models of human disease. 640 5