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Effect of L-Carnitine on Acetyl-CoA Content and Activity of Blood Platelets in Healthy and Diabetic Persons

Anna Michno¹, Anna Raszeja-Specht¹, Agnieszka Jankowska-Kulawy¹, Tadeusz Paweczyk² and Andrzej Szutowicz^1,a

Chair of Clinical Biochemistry, Departments of¹ Laboratory Medicine and ² Molecular Medicine, Medical University of Gdask, Gdask, Poland.

^aAddress correspondence to this author at: Department of Laboratory Medicine, Medical University of Gdask, Dbinki 7, 80-211 Gdask, Poland. Fax 48-58-349-2784; e-mail szut{at}amg.gda.pl.

Background: Excessive blood platelet activity contributes to vascular complications in diabetic persons. Increased acetyl-CoA in platelets from diabetic persons has been suggested to be a cause of this hyperactivity. We therefore investigated whether L-carnitine, which up-regulates metabolism of acetyl-CoA in muscles and brain, may affect platelet function in healthy and diabetic individuals.

Methods: We obtained platelets from healthy and diabetic persons and measured acetyl-CoA concentrations, malonyl dialdehyde (MDA) synthesis, and platelet aggregation in the absence and presence of L-carnitine. Activities of selected enzymes involved in glucose and acetyl-CoA metabolism were also assessed.

Results: Fasting glucose, fructosamine, and hemoglobin A_1c were present in significantly higher amounts in the blood of diabetic patients than in healthy individuals. Activities of carnitine acetyltransferase, glucose-6-phosphate dehydrogenase, oxoglutarate dehydrogenase, and fatty acid synthase were 17%–62% higher in platelets from diabetic patients. Mitochondrial acetyl-CoA was increased by 98% in platelets from diabetic patients, MDA synthesis was increased by 73%, and platelet aggregation by 60%. L-Carnitine had no or only a slight effect on these indices in platelets from healthy individuals, but in platelets from diabetic patients, L-carnitine caused a 99% increase in acetyl-CoA in the cytoplasmic compartment along with increases in MDA synthesis and platelet aggregation.

Conclusions: Excessive platelet activity in persons with diabetes may result from increased acetyl-CoA, which apparently increases synthesis of lipid activators of platelet function. L-Carnitine may aggravate platelet hyperactivity in diabetic persons by increasing the provision of surplus acetyl-CoA to the cytoplasmic compartment.

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				A. Michno, H. Bielarczyk, T. Pawelczyk, A. Jankowska-Kulawy, J. Klimaszewska, and A. Szutowicz Alterations of Adenine Nucleotide Metabolism and Function of Blood Platelets in Patients With Diabetes Diabetes, February 1, 2007; 56(2): 462 - 467. [Abstract] [Full Text] [PDF]

				G. D'Argenio, M. Calvani, A. Casamassimi, O. Petillo, S. Margarucci, M. Rienzo, I. Peluso, R. Calvani, A. Ciccodicola, N. Caporaso, et al. Experimental colitis: decreased Octn2 and Atb0+ expression in rat colonocytes induces carnitine depletion that is reversible by carnitine-loaded liposomes FASEB J, December 1, 2006; 20(14): 2544 - 2546. [Abstract] [Full Text] [PDF]