Diabetes, Insulin, Tolbutamide, and Glucose Load in the Degradation of C-14-labeled Lactate and Pyruvate

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Abstract
In 2 insulin-dependent diabetic patients, mild ketoacidosis was accompanied by a decrease in the formation of C-14-02 from DL-lactate-2-C-14 to about 2/3 of the values obtained when the patients were in good control. One patient received the labeled compound by single intravenous injection in trace amount and the other by intravenous infusion with a load of DL-sodium lactate. Prior intravenous administration of insulin in these 2 patients caused no increase in output of C-14-O2 above that in the control state, and a minor, insignificant increase in 2 milder diabetic patients (one given DL-lactate-2-C-14 with an infusion of glucose, the other DL-lactate-2-C-14 without glucose). The activity of C-14 in expired carbon dioxide of diabetic patients (in good control) was 10 to 25% less than that of one nondiabetic subject after administration of DL-lactate-2-C-14. In the latter patient, and in another nondiabetic given pyruvate-2-C-14, the rapid intranveous injection of 25 g of glucose 20 min. before the labeled compound was accompanied by more rapid and extensive formation of C-14-O2 than in the fasting state. Tolbutamide in 2 studies (one with DL-lactate-2-C-14 and a prior glucose load in a nondiabetic, and the other with DL-lactate-3-C-14 in a mild diabetic) had no apparent effect on the formation of C-14-O2. Comparison of lactate-2-C-14 with lactate-3-C-14 in one diabetic patient showed 50% higher specific activity of C-14-O2 from the former labeled compound. Studies of the concentration of lactic acid in the blood and rate of disappearance of DL-lactate-2-C-14 further indicated mild lactic acidemia which was associated with decreased elimination of lactic acid-C-14 from the blood of these diabetic patients.