Baker N
Fed Proc. 1977 Feb;36(2):253-8.
Tracer experiments have been carried out using gorging and nibbling mice to study several related aspects of carbohydrate metabolism: 1) inhibition of gluconeogenesis shortly after animals ingest a glucose-rich meal; 2) the extent to which dietary glucose carbon is recycled by way of 3C compounds after dietary glucose is absorbed; and 3) recycling of glucose by exchange between free and a hypothetical, "bound" glucose pool. Fasted, gorging mice were allowed to eat 120 mg [U-14C,6-T]glucose (58% glucose diet) in 4 min. Plasma glucose-C specific activity rapidly reached that of the dietary glucose-C. Superficially, this suggested nearly complete inhibition of hepatic gluconeogenesis. However, plasma [6-T]glucose, glycogen-[14C, 3H]glucose analyses, and [14C]-glycerol conversion to glucose showed that hepatic gluconeogenesis continued during alimentary hyperglycemia. Half of liver glycogen seemed to be formed from a hepatic G-6-P pool that was never labeled. Indirect kinetic evidence of a large, bound exchangeable glucose pool was presented. Since no direct evidence of such a pool has been obtained, the possibility is raised that a serious artifact of the tracer technique exists or else some unconventional model of carbohydrate metabolism is required to explain our data.
已经使用贪食和少食的小鼠进行了示踪实验，以研究碳水化合物代谢的几个相关方面：1）动物摄入富含葡萄糖的食物后不久糖异生的抑制；2）膳食葡萄糖被吸收后，膳食葡萄糖碳通过三碳化合物循环的程度；3）通过游离葡萄糖池和假设的“结合”葡萄糖池之间的交换实现葡萄糖的循环。禁食的贪食小鼠在4分钟内被允许食用120毫克[U-14C,6-T]葡萄糖（58%葡萄糖饮食）。血浆葡萄糖-C比活性迅速达到膳食葡萄糖-C的比活性。表面上，这表明肝脏糖异生几乎完全受到抑制。然而，血浆[6-T]葡萄糖、糖原-[14C, 3H]葡萄糖分析以及[14C]-甘油转化为葡萄糖表明，在食后高血糖期间肝脏糖异生仍在继续。肝脏糖原的一半似乎由从未被标记的肝脏G-6-P池形成。提出了一个大的、结合的可交换葡萄糖池的间接动力学证据。由于尚未获得这种池的直接证据，因此有可能存在示踪技术的严重假象，或者需要一些非常规的碳水化合物代谢模型来解释我们的数据。
