Erythrocyte O₂ Transport and Metabolism and Effects of Vitamin B₆ Therapy in Type II Diabetes Mellitus Free

The effects of vitamin B₆ on erythrocyte metabolism, erythrocyte hemoglobin O₂ affinity (P50), and nonenzymatic glycosylation were studied in 15 Caucasian men with type II (non-insulin-dependent) diabetes mellitus. A control group of 13 healthy Caucasian men was also evaluated. Before treatment, diabetic subjects had low mean cell hemoglobin concentration values and increases in both erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels and erythrocyte hexokinase activities. Although all three of these changes are associated with a decrease in hemoglobin O₂ (Hb-O₂) affinity, P50 values were normal in diabetic subjects. Moreover, P50 values normalized to pH 7.4 (P50_7.4) were inversely related to the level of glycosylated hemoglobin (HbA_1c). Both erythrocyte 2,3-DPG and erythrocyte ATP were also inversely related to HbA_1c. Vitamin B₆ nutriture, as determined by erythrocyte aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, was normal in all diabetic subjects before vitamin B₆ therapy. Nonetheless, HbA_1c levels decreased after 6 wk of treatment with 150 mg/day pyridoxine and increased again during placebo administration. These changes were not explained by changes in fasting blood glucose. Pyridoxine therapy also decreased P50_7.4values and increased erythrocyte AST and ALT activities but had no effect on 2,3-DPG, ATP, or the activities of hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. These observations suggest that 1) nonenzymatic glycosylation may play a role in regulating both erythrocyte metabolism and Hb-O₂affinity in diabetic subjects, and 2) vitamin B₆ therapy may modify nonenzymatic glycosylation of hemoglobin in this population.