In two insulin-dependent diabetic patients, mild ketoacidosis was accompanied by a decrease in the formation of C-14-O2 from DL-lactate-2-C-14 to about two thirds 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 two patients caused no increase in output of C-14-O2 above that in the control state, and a minor, insignificant increase in two 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 per cent 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 intravenous injection of 25 gm. of glucose twenty minutes before the labeled compound was accompanied by more rapid and extensive formation of C-14-O2 than in the fasting state. Tolbutamide in two 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 per cent 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.

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