Newgard C B, Hirsch L J, Foster D W, McGarry J D
J Biol Chem. 1983 Jul 10;258(13):8046-52.
To quantify the extent to which exogenous glucose is used directly or indirectly for hepatic glycogen synthesis, fasted rats were given [U-14C,3-3H] glucose intragastrically, intravenously, or as a component of a solid diet eaten ad libitum. In all cases liver glycogen was deposited at high linear rates over a 3-h period. Portal vein glucose levels seldom exceeded 8 mM. At a time when the specific activities of 3H and 14C in circulating glucose were identical with those in the administered material their values in newly synthesized glycogen were reduced by 72-88% and 50-65%, respectively. An intragastric load of unlabeled glucose sufficient to suppress completely hepatic glucose output greatly stimulated the incorporation of intravenously infused [14C]bicarbonate, [14C]lactate, [14C]alanine, and [14C] glutamine into liver glycogen. Using an improved assay the ability of liver homogenates to phosphorylate glucose at concentrations of 5-10 mM was found to be far short of what would be needed if glucose were used directly to support hepatic glycogen synthesis in vivo. These data support the notion that in the rat a major fraction of liver glycogen deposited in response to exogenous carbohydrate is formed by a pathway involving glucose leads to C3 unit leads to glycogen, although the site of the initial steps in the sequence is not yet known. The limited capacity of the liver to utilize intact glucose for glycogen synthesis might reside in its limited capacity to phosphorylate the sugar at physiological concentrations.
为了量化外源性葡萄糖直接或间接用于肝糖原合成的程度,对禁食大鼠经胃内、静脉内给予[U-14C,3-3H]葡萄糖,或将其作为随意进食的固体饮食的一部分给予。在所有情况下,肝糖原在3小时内以高线性速率沉积。门静脉葡萄糖水平很少超过8 mM。当循环葡萄糖中3H和14C的比活度与给药物质中的比活度相同时,它们在新合成糖原中的值分别降低了72 - 88%和50 - 65%。足以完全抑制肝葡萄糖输出的未标记葡萄糖胃内负荷极大地刺激了静脉输注的[14C]碳酸氢盐、[14C]乳酸盐、[14C]丙氨酸和[14C]谷氨酰胺掺入肝糖原。使用一种改进的测定方法发现,肝匀浆在5 - 10 mM浓度下磷酸化葡萄糖的能力远远低于体内直接使用葡萄糖来支持肝糖原合成所需的能力。这些数据支持这样一种观点,即在大鼠中,响应外源性碳水化合物而沉积的大部分肝糖原是通过一条涉及葡萄糖→C3单位→糖原的途径形成的,尽管该序列中初始步骤的位点尚不清楚。肝脏利用完整葡萄糖进行糖原合成的能力有限可能在于其在生理浓度下磷酸化该糖的能力有限。