Received on March 1, 2005
Accepted on June 7, 2005

Endocrinology and Metabolism

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

Anna Michno ¹, Anna Raszeja-Specht ¹, Agnieszka Jankowska-Kulawy ¹, Tadeusz Paweczyk ², Andrzej Szutowicz ^1*

¹ Laboratory Medicine, Medical University of Gdask, Gdask, Poland
² Molecular Medicine, Medical University of Gdask, Gdask, Poland

^* To whom correspondence should be addressed. 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. provide

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.