Rofe A M, James H M, Bais R, Edwards J B, Conyers R A
Aust J Exp Biol Med Sci. 1980 Apr;58(2):103-16. doi: 10.1038/icb.1980.10.
Oxalate (14C) was produced during the metabolism of (U-14C) carbohydrates in hepatocytes isolated from normal rats. At 10 mM, the order of oxalate production was fructose > glycerol > xylitol > sorbitol greater than or equal to glucose in the ratio 10 : 4 : 3 : 1 : 1. This difference between oxalate production from fructose and glucose was reflected in their rates of utilisation, glucose being poorly metabolised in hepatocytes from fasted rats. Fructose was rapidly metabolised, producing glucose, lactate and pyruvate as the major metabolites. Glycerol, xylitol and sorbitol were metabolised at half the rate of fructose, the major metabolites being glucose, lactate and glycerophosphate. The marked similarity in the pattern of intermediary metabolites produced by these polyols was not, however, reflected in the rates of oxalate production. Hepatic polyol metabolism resulted in high levels of cytosolic NADH, as indicated by elevated lactate : pyruvate and glycerophosphate : dihydroxyacetone phosphate ratios. The artificial electron acceptor, phenazine methosulphate (PMS) stimulated oxalate production from the polyols, particularly xylitol. In the presence of PMS, the order of oxalate production was fructose greater than or equal to xylitol > glycerol > sorbitol in the ratio 10 : 10 : 6 : 2. The production of glucose, lactate and pyruvate from the polyols was also stimulated by PMS, whereas the general metabolism of fructose, including oxalate production, was little affected. Oxalate (14C) was produced from (1-14C), (2-14C) and (6-14C) but not (3,4-14C) glucose in hepatocytes isolated from non-fasted, pyridoxine-deficient rats. Whilst this labelling pattern is consistent with oxalate being produced by a number of pathways, it is suggested that metabolism via hydroxypyruvate is a major route for oxalate production from various carbohydrates, with perhaps the exception of xylitol, which appears to have an alternative mechanism for oxalate production. The observation that carbohydrates, particularly fructose, contribute to endogenous oxalate production lends support to the hypothesis that a high sucrose consumption contributes to the formation of renal oxalate stones in man.
在从正常大鼠分离的肝细胞中，（U-14C）碳水化合物代谢过程中产生了草酸盐（14C）。在10 mM浓度下，草酸盐产生的顺序为果糖>甘油>木糖醇>山梨醇≥葡萄糖，比例为10:4:3:1:1。果糖和葡萄糖产生草酸盐的差异反映在它们的利用速率上，禁食大鼠肝细胞中葡萄糖的代谢较差。果糖迅速代谢，产生葡萄糖、乳酸和丙酮酸作为主要代谢产物。甘油、木糖醇和山梨醇的代谢速率是果糖的一半，主要代谢产物为葡萄糖、乳酸和甘油磷酸。然而，这些多元醇产生的中间代谢产物模式的显著相似性并未反映在草酸盐产生的速率上。肝脏多元醇代谢导致细胞溶质NADH水平升高，乳酸:丙酮酸和甘油磷酸:磷酸二羟丙酮比值升高表明了这一点。人工电子受体吩嗪硫酸甲酯（PMS）刺激了多元醇产生草酸盐，特别是木糖醇。在PMS存在下，草酸盐产生的顺序为果糖≥木糖醇>甘油>山梨醇，比例为10:10:6:2。PMS也刺激了多元醇产生葡萄糖、乳酸和丙酮酸，而果糖的一般代谢，包括草酸盐产生，几乎没有受到影响。在从非禁食、吡哆醇缺乏大鼠分离的肝细胞中，草酸盐（14C）由（1-14C）、（2-14C）和（6-14C）葡萄糖产生，但不由（3,4-14C）葡萄糖产生。虽然这种标记模式与草酸盐通过多种途径产生一致，但有人认为，通过羟基丙酮酸的代谢是各种碳水化合物产生草酸盐的主要途径，可能木糖醇除外，木糖醇似乎有另一种草酸盐产生机制。碳水化合物，特别是果糖，有助于内源性草酸盐产生这一观察结果支持了高蔗糖消耗导致人类肾草酸结石形成的假说。
