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

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 (TXB2) and prostacyclin (PGI(2)) were measured. In healthy volunteers (age, 42 +/- 11 years; BMI, 28.4 +/- 4.8 k g/m(2); n = 28), the ingestion of G. biloba extract significantly increased fasting insulin and C-peptide (10 4 vs. 12 +/- 6 muU/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-TXB2 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(1 alpha) and 6-keto-PGF(1 alpha)) 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 k g/m(2); n = 19), G. biloba ingestion did not affect pancreatic beta-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. (C) 2002 Elsevier Science Ltd. All rights reserved.