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Results for “LIVER GLYCOGEN”

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PubMed1978

Frog liver glycogen synthase. In vitro and in vivo interconversions between I and D forms.

1. Frog liver has enzymatic systems able to interconvert glycogen synthase. 2. D to I conversion is achieved in vitro by incubation at 30 degrees C. ATP, ADP, inorganic phosphate and glycogen are inhibitors of this conversion, whereas glucose-6-P and Mg2+ stimulate it. 3. I to D conversion in vitro depends on ATP-Mg2+. Cyclic-AMP activates this conversion, while glucose-6-P inhibits it. 4. Injection of glucose, ribose, mannose, fructose, galactose, and cortisone into frogs increase liver percentage of I activity. 5. Glucagon and adrenaline decrease percentage of I activity.

Animals↗
PubMed1995

Mutations in the phosphorylase kinase gene PHKA2 are responsible for X-linked liver glycogen storage disease.

Phosphorylase kinase (PHK) is a key enzyme in the control of glycogen breakdown. Several types of PHK deficiency have been described of which X-linked liver glycogenosis type I (XLG I) is the most common. Since the XLG I locus and the gene encoding the liver alpha-subunit gene of PHK (PHKA2) have both been localized to Xp22, PHKA2 was a candidate gene for XLG I. In this study we identified four point mutations in four unrelated XLG I patients: three mutations introduce a premature stop codon, whereas the fourth mutation abolishes a splice site consensus sequence leading to exon skipping. These findings indicate that PHKA2 is the XLG I gene.

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