Searle G L, Siperstein M D
Diabetes. 1975 Aug;24(8):741-5. doi: 10.2337/diab.24.8.741.
Using uniformly labeled 14C L-lactate, we have studied the turnover and oxidation of lactic acid in a patient who presented with a mild lactic acidosis while on phenformin medication. As with other cases of lactic acidosis associated with phenformin therapy, this subject had impaired renal function as evidenced by serum creatinine levels of 2 mg./100 ml. and BUNs of 40 mg./100 ml. Comparison of the rate of lactate oxidation relative to the rate of lactate turnover in this subject while on and off phenformin therapy suggests that a prime factor leading to the elevated lactate levels in this situation in impaired peripheral aerobic metabolism. Although lactate oxidation was increased in the presence of phenformin, the control studies clearly demonstrate that aerobic metabolism was not keeping pace with the increased level of anaerobic carbohydrate metabolism brought on by the drug. It is concluded that it is this imbalance in lactate metabolism that is responsible for the lactic acidosis that accompanies phenformin therapy.
我们使用均匀标记的14C L-乳酸盐，研究了一名在服用苯乙双胍药物时出现轻度乳酸酸中毒患者体内乳酸的周转和氧化情况。与其他与苯乙双胍治疗相关的乳酸酸中毒病例一样，该患者肾功能受损，血清肌酐水平为2毫克/100毫升，血尿素氮为40毫克/100毫升。对该患者在服用和停用苯乙双胍治疗期间乳酸氧化速率与乳酸周转速率的比较表明，导致这种情况下乳酸水平升高的一个主要因素是外周有氧代谢受损。尽管在苯乙双胍存在的情况下乳酸氧化增加，但对照研究清楚地表明，有氧代谢跟不上该药物引起的无氧碳水化合物代谢增加的水平。得出的结论是，正是这种乳酸代谢的不平衡导致了苯乙双胍治疗伴随的乳酸酸中毒。
