The liver plays a key role for the maintenance of blood glucose homeostasis under widely changing physiological conditions. In the overnight fasted state, breakdown of hepatic glycogen and synthesis of glucose from lactate, amino acids, glycerol, and pyruvate contribute about equally to hepatic glucose production. Postprandial glucose uptake by the liver is determined by the size of the glucose load reaching the liver, the rise in insulin concentration, and the route of glucose delivery. Hepatic glycogen stores are depleted within 36 to 48 hours of fasting, but gluconeogenesis continues to provide glucose for tissues with an obligatory glucose requirement. Glucose output from the liver increases during exercise; during short-term intensive exertion, hepatic glycogenolysis is the primary source of extra glucose for skeletal muscle, and during prolonged exercise, hepatic gluconeogenesis becomes gradually more important in keeping with falling insulin and rising glucagon levels. Type 1 diabetes is accompanied by diminished hepatic glycogen stores, augmented gluconeogenesis, and increased basal hepatic glucose production in proportion to the severity of the diabetic state. The hyperglycemia of type 2 diabetes is in part caused by an overproduction of glucose from the liver that is secondary to accelerated gluconeogenesis.

中文翻译：

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内脏调节葡萄糖的产生。

在广泛变化的生理条件下，肝脏对于维持血糖稳态起着关键作用。在过夜禁食状态下，肝糖原分解和由乳酸，氨基酸，甘油和丙酮酸合成葡萄糖对肝葡萄糖生成的贡献大致相同。餐后肝脏对葡萄糖的摄取取决于到达肝脏的葡萄糖负荷量，胰岛素浓度的升高以及葡萄糖输送的途径。禁食后36至48小时内肝糖原存储被耗尽，但是糖异生继续为需要葡萄糖的组织提供葡萄糖。运动过程中肝脏的葡萄糖输出增加；在短期密集运动中，肝糖原分解是骨骼肌多余葡萄糖的主要来源，在长时间的运动中，随着胰岛素的下降和胰高血糖素水平的升高，肝糖异生逐渐变得越来越重要。1型糖尿病伴有肝糖原储存减少，糖异生增加和基础肝葡萄糖生成增加（与糖尿病状态的严重程度成比例）。2型糖尿病的高血糖部分是由于肝脏中葡萄糖的过度产生所致，而葡萄糖过高是继发于糖原异生的继发因素。