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PubMed2001

Case report: liver glycogen synthase deficiency--a cause of ketotic hypoglycemia.

Glycogen synthase deficiency is a rare inborn error of metabolism, characterized by fasting hypoglycemia, hypoglycemic seizures, and ketonuria. Only 7 families with 14 affected children have been reported. Here, we report an additional patient with this deficiency. Findings in this patient were clinically and biochemically consistent with those reported in patients with ketotic hypoglycemia and may alert the clinician to consider glycogen synthase deficiency.

Female↗
PubMed1980

[The hormonal regulation of the hepatic glycogenolysis in the newborn (author's transl)].

Through the hepatic glycogenolysis is the most important metabolism for energy source, the hormonal regulation in neonate is unknown yet. The neonatal rats were investigated chronologically in regard to liver wet weight, blood glucose, liver glycogen, liver glucose and liver cyclic AMP. And the influence of epinephrine and glucagon on the glycogenolysis were observed using isolated perifused rat liver. As a result, following conclusions were drawn. 1. In the earlier neonate, the source of the blood glucose mainly depended on the liver glycogen restored before birth. In the later neonate, the liver glycogen was reaccumulated by the progression of the suckling. 2. Although, in the earlier neonate, the influence of epinephrine on the glycogenolysis was more dominant than that of glucagon, the hepatic glycogenolysis was completely established by both hormones since the fifth day from birth. 3. In respect to the glucose output of liver, it was regulated by the interaction of these two hormones chronologically. 4. In the hepatic glycogenolysis of the neonates, just like that of the adults, cyclic AMP was also the second messenger of epinephrine and glucagon. 5. The third day after birth in the neonate was the critical period in the carbohydrate metabolism.

Age Factors↗
PubMed1992

[Regulation of glycogen metabolism in liver].

Glycogen metabolism in the liver is subject to complex regulations in which substrates or hormones may interact in different ways according to the nutritional conditions. Activation of glycogen synthesis strongly depends on the availability of glucose, gluconeognic substrates and amino acids. These factors act mainly by a direct or indirect activation of the synthase phosphatase. On the other hand, cAMP or Ca(2+)-dependent glycogenolytic agents cause glycogen degradation by the mean of specific protein kinases which may inactivate the glycogen synthase or activate the glycogen phosphorylase. The active form of glycogen phosphorylase is a potent allosteric inhibitor of the synthase phosphatase. Insulin increases glycogen synthesis by counteracting the action of glycogenolytic hormones and by enhancing the glucose induced activation of glycogen synthase. The respective importance of these different regulations is discussed in this article.

Animals↗