TY - JOUR
T1 - Effect of the ingestion of Ginkgo biloba extract on platelet aggregation and urinary prostanoid excretion in healthy and Type 2 diabetic subjects
AU - Kudolo, George B.
AU - Dorsey, Sheryl
AU - Blodgett, Janet
N1 - Funding Information:
The nursing and dietetic care provided by the staff of the Frederic C. Bartter GCRC at the South Texas Veterans Health Care Systems, Audie Murphy Division is appreciated. The study was supported by NIH grants M01-RR-01346 and R01 AT-00832-01 and funds from the Kronkosky Charitable Foundation.
PY - 2002/11/1
Y1 - 2002/11/1
N2 - 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 B2 (TXB2) and prostacyclin (PGI2) were measured. In healthy volunteers (age, 42±11 years; BMI, 28.4±4.8 kg/m2; 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-TXB2 from 12.4±6.1 to 10.3±6.1 ng/mg Cr (p<0.04) and PGI2 metabolites (2,3-dinor-6-keto-PGF1α and 6-keto-PGF1α) 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/m2; 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 TXA2 in platelets and COX-2-mediated PGI2 production by the endothelial cells and perhaps platelet-enriched levels of arachidonic acid or COX-1 activity, or both, in T2DM subjects.
AB - 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 B2 (TXB2) and prostacyclin (PGI2) were measured. In healthy volunteers (age, 42±11 years; BMI, 28.4±4.8 kg/m2; 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-TXB2 from 12.4±6.1 to 10.3±6.1 ng/mg Cr (p<0.04) and PGI2 metabolites (2,3-dinor-6-keto-PGF1α and 6-keto-PGF1α) 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/m2; 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 TXA2 in platelets and COX-2-mediated PGI2 production by the endothelial cells and perhaps platelet-enriched levels of arachidonic acid or COX-1 activity, or both, in T2DM subjects.
KW - Diabetes
KW - Ginkgo biloba
KW - Platelet aggregation
KW - Prostacyclin
KW - Thromboxane
UR - http://www.scopus.com/inward/record.url?scp=0036878140&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036878140&partnerID=8YFLogxK
U2 - 10.1016/S0049-3848(02)00394-8
DO - 10.1016/S0049-3848(02)00394-8
M3 - Article
C2 - 12590952
AN - SCOPUS:0036878140
SN - 0049-3848
VL - 108
SP - 151
EP - 160
JO - Thrombosis Research
JF - Thrombosis Research
IS - 2-3
ER -