其中一共有12名儿童(5%)(8名女童，4名男童)患有糖原累积病而药物治疗无效。
A total of 12 (5%) children (8 female and 4 male) were afflicted with GSD and were not responsive to medical treatment.
通过组织化学的方法，观察了用碳酸锂处理四氧嘧啶性糖尿病大鼠3周后肝糖原含量的变化。
By the method of histochemistry, effect of lithium carbonate on hepatic glycogen was observed after 3 weeks of administration of lithium carbonate to diabetic rats induced by alloxan.
结果：实验组与糖尿病对照组相比，肝细胞糖原含量增多。
RESULTS: Compared experimental group with diabetic control group, content of liver starch was increased.
通过腹腔注射四氧嘧啶造小鼠糖尿病模型，观察血糖、肝糖原、葡萄糖激酶等指标。
An experimental diabetes model was produced by intraperitoneal injection of alloxan. Blood glucose, liver glucokinase and liver glycogen contents were measured.
背景-PRKAG2突变引起糖原贮积型心肌病，心室预激和传导系统退化。
Background-PRKAG2 mutations cause glycogen-storage cardiomyopathy, ventricular preexcitation, and conduction system degeneration.
方法：建立四氧嘧啶糖尿病小鼠动物模型，测定肝脏抗氧化酶、ATP酶活性、脂质过氧化产物、一氧化氮(NO)和肝糖原含量。
METHODS: the model of alloxan diabetic mice was established to determined the activities of enzymes of antioxidant and ATP, and the contents of MDA, NO and glycogenesis.
方法：建立四氧嘧啶糖尿病小鼠动物模型，测定肝脏抗氧化酶、ATP酶活性、脂质过氧化产物、一氧化氮(NO)和肝糖原含量。
METHODS: the model of alloxan diabetic mice was established to determined the activities of enzymes of antioxidant and ATP, and the contents of MDA, NO and glycogenesis.
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