Effect of the ingestion of Ginkgo biloba extract on platelet aggregation and urinary prostanoid excretion in healthy and Type 2 diabetic subjects

Abstract

Enhanced platelet function, particularly in response to collagen, is a common occurrence in diabetes that increases the risk of cardiovascular disease. Ginkgo biloba extract is ingested primarily to improve mental focus but it possesses a blood-thinning potential, which has not been well characterized. This study was designed to compare the effect of ingesting G. biloba extract on platelet aggregation in platelet-rich plasma (PRP) and prostanoid urinary excretion in healthy volunteers and subjects with Type 2 diabetes mellitus (T2DM). Before and after ingesting 120 mg of standardized G. biloba extract for 3 months, platelet aggregation was studied in PRP and urinary metabolites of thromboxane B 2 (TXB 2) and prostacyclin (PGI 2) were measured. In healthy volunteers (age, 42±11 years; BMI, 28.4±4.8 kg/m 2; n=28), the ingestion of G. biloba extract significantly increased fasting insulin and C-peptide (10±4 vs. 12±6 μU/ml, p<0.007 and 1.3±0.8 vs. 2.1±1.1 ng/ml, p<0.001, respectively) and significantly reduced collagen but not PAF-mediated platelet aggregation, converting 21 of 28 subjects with [COL+/EPI+] platelets to the [COL−/EPI+] phenotype. This was accompanied by a reduction of 11-dehydro-TXB 2 from 12.4±6.1 to 10.3±6.1 ng/mg Cr ( p<0.04) and PGI 2 metabolites (2,3-dinor-6-keto-PGF 1α and 6-keto-PGF 1α) from 2.2±0.8 to 1.8±0.8 ng/mg Cr ( p<0.05). In the T2DM subjects (age, 54±8; BMI, 36.6±7.9 kg/m 2; n=19), G. biloba ingestion did not affect pancreatic β-cell function but significantly reduced platelet aggregation, converting 16 of 19 [COL+/EPI+] platelets to the [COL−/EPI+] phenotype. Unlike the healthy volunteers, this was not accompanied by a reduced urinary prostanoid excretion. G. biloba-induced reduction of both classes of prostanoid metabolites in healthy volunteers, but not in T2DM subjects, may suggest a nonselective inhibition of COX-1-mediated TXA 2 in platelets and COX-2-mediated PGI 2 production by the endothelial cells and perhaps platelet-enriched levels of arachidonic acid or COX-1 activity, or both, in T2DM subjects.