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Alterations of Adenine Nucleotide Metabolism and Function of Blood Platelets in Patients With Diabetes

Anna Michno¹, Hanna Bielarczyk¹, Tadeusz Paweczyk², Agnieszka Jankowska-Kulawy¹, Joanna Klimaszewska¹, and Andrzej Szutowicz¹

¹ Chair of Clinical Biochemistry, Department of Laboratory Medicine, Medical University of Gdask, Gdask, Poland
² Department of Molecular Medicine, Medical University of Gdask, Gdask, Poland

Address correspondence and reprint requests to Andrzej Szutowicz, Department of Laboratory Medicine, Medical University of Gdask, Dêbinki 7, 80-211 Gdask, Poland. E-mail: aszut{at}amg.gda.pl

Abbreviations: GPRP, glycine-proline-arginine-proline-NH₂; TBARS, thiobarbituric acid–reactive species

Increased activity of blood platelets contributes to vascular complications in patients with diabetes. The aim of this work was to investigate whether persisting hyperglycemia in diabetic patients generates excessive accumulation of ATP/ADP, which may underlie platelet hyperactivity. Platelet ATP and ADP levels, thiobarbituric acid–reactive species synthesis, and aggregation of platelets from patients with diabetes were 18–82% higher than in platelets from healthy participants. In patients with diabetes, platelet stimulation with thrombin caused about two times greater release of ATP and ADP than in the healthy group while decreasing intraplatelet nucleotide content to similar levels in both groups. This indicates that the increased content of adenylate nucleotides in the releasable pool in the platelets of diabetic patients does not affect their level in metabolic cytoplasmic/mitochondrial compartments. Significant correlations between platelet ATP levels and plasma fructosamine, as well as between platelet ATP/ADP and platelet activities, have been found in diabetic patients. In conclusion, chronic hyperglycemia-evoked elevations of ATP/ADP levels and release from blood platelets of patients with diabetes may be important factors underlying platelet hyperactivity in the course of the disease.

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