Shames D M, Berman M, Segal S
J Clin Invest. 1971 Mar;50(3):627-41. doi: 10.1172/JCI106533.
Glucose oxidation to CO(2) in man at the fasted, steady state has been investigated in normal, hypothyroid, patients by monitoring the specific activity of plasma glucose and expired CO(2) after intravenous injection of glucose-1-(14)C, glucose-6-(14)C, and sodium bicarbonate-(24)C in tracer amounts. Making certain stoichiometric assumptions about the oxidation of the C-1 and C-6 carbons of glucose to CO(2), the data are incorporated into a multicompartmental model describing the kinetics of plasma glucose, plasma bicarbonate, and the conversion of glucose to CO(2) by the hexose monophosphate pathway and all other series and parallel pathways which oxidize glucose carbon to CO(2) (EMP-TCA). This formulation separates the distribution kinetics of glucose and bicarbonate from the kinetics of glucose oxidation to CO(2). It allows the calculation of a minimal fraction (varphi(t)) of glucose irreversibly oxidized to CO(2) which is based entirely on the duration of the experimental data. This calculation is independent of the extrapolative implications of the model beyond the experimental interval and of the particular model chosen to fit the data. All modeling and data fitting were performed on a digital computer with the SAAM program. Based on a 300 min experiment the analysis suggests that in hypothyroidism there is a decrease in the rate of glucose metabolized irreversibly (rhoG). There is also a decrease in the minimal fraction (varphi(300)) which is completely oxidized to CO(2) by way of the EMP-TCA. rhoG and varphi(300) are 0.56 and 0.42 mmole/min respectively as compared to 0.89 and 0.50 mmole/min respectively in normals. However, the fraction of the C-1 of glucose metabolized irreversibly which undergoes oxidation to CO(2) by the hexose monophosphate pathway (Psi) is not different from normal (0.07 and 0.07 respectively). The hyperthyroid studies suggest that rhoG and varphi(300) are within the normal range (1.01 and 0.46 mmoles/min respectively as compared to 0.89 and 0.50 mmole/min respectively in normals). However, Psi is decreased to less than half the normal value (0.03 as compared to 0.07 in normals).
通过静脉注射微量的1-(14)C葡萄糖、6-(14)C葡萄糖和(24)C碳酸氢钠后，监测血浆葡萄糖和呼出二氧化碳的比活性，对正常、甲状腺功能减退患者在禁食、稳定状态下人体葡萄糖氧化为二氧化碳的情况进行了研究。在对葡萄糖的C-1和C-6碳氧化为二氧化碳做了某些化学计量学假设后，将数据纳入一个多室模型，该模型描述了血浆葡萄糖、血浆碳酸氢盐的动力学，以及通过磷酸己糖途径和所有其他将葡萄糖碳氧化为二氧化碳的串联和平行途径（糖酵解-三羧酸循环）将葡萄糖转化为二氧化碳的过程。这种公式将葡萄糖和碳酸氢盐的分布动力学与葡萄糖氧化为二氧化碳的动力学区分开来。它允许计算完全基于实验数据持续时间的、不可逆氧化为二氧化碳的葡萄糖的最小分数（varphi(t)）。该计算与模型在实验区间之外的外推含义以及为拟合数据而选择的特定模型无关。所有建模和数据拟合均使用SAAM程序在数字计算机上进行。基于300分钟的实验分析表明，甲状腺功能减退时不可逆代谢的葡萄糖速率（rhoG）降低。通过糖酵解-三羧酸循环完全氧化为二氧化碳的最小分数（varphi(300)）也降低。rhoG和varphi(300)分别为0.56和0.42毫摩尔/分钟，而正常人分别为0.89和0.50毫摩尔/分钟。然而，通过磷酸己糖途径不可逆代谢的葡萄糖C-1中氧化为二氧化碳的分数（Psi）与正常情况无异（分别为0.07和0.07）。甲状腺功能亢进的研究表明，rhoG和varphi(300)在正常范围内（分别为1.01和0.46毫摩尔/分钟，而正常人分别为0.89和0.50毫摩尔/分钟）。然而，Psi降至正常价值的一半以下（0.03，而正常人是0.07）。
