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Abstract
As early as in 19 39 Guest and Rapoport reported a striking decrease of the red cell 2,3-diphosphoglycerate (2,3-DPG) concentration in patients suffering from severe diabetic ketoacidosis (1). This observation has been amply confirmed in more recent years (2,3,4,5), when interest was resurrected to investigate the regulation of red cell 2,3-DPG after Benesch and Benesch (6) and Chanutin and Curnish (7) had shown the effect of 2,3-DPG on the oxygen affinity of hemoglobin. 2,3-DPG is formed as an intermediary product of red cell glycolysis; increase in hydrogen-ion concentration decreases red cell glycolysis mainly through inhibition of the phosphofructokinase step (8) and it has been widely accepted that the remarkable low erythrocyte 2,3-DPG levels in diabetic ketoacidosis — as little as 2o per cent of the normal concentration is observed — are due to this mechanism and an additional inhibition of di-phosphoglycerate mutase at lower pH (9).
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