Herbal remedy is popular among those with chronic diseases, who may already be taking several prescription medications, thereby increasing the risk of drug-herb interactions. Ginkgo biloba extract is a popular dietary supplement that is ingested by the general population to enhance mental focus and by the elderly to delay onset of age-acquired loss of cognitive function. In subjects with non-insulin dependent diabetes (NIDDM), ingestion of Ginkgo biloba significantly increases pancreatic beta-cell function. The increased plasma C-peptide levels in response to glucose loading is accompanied by decreased plasma insulin levels and no significant changes in plasma glucose levels. The central hypothesisof this application is that ingestion of Ginkgo biloba produces the dissimilar plasma C-peptide/insulin ratios by increasing the metabolic clearance rates of insulin and the antidiabetic medications. The underlying mechanism may involve the alteration of drug pharmacokinetics resulting in decreased efficacy of the hypoglycemic agents and increased whole body insulin resistance. The primary objective-of this study is to determine the mechanism by which Ginkgo biloba may accelerate pancreatic function and reduce glucose metabolism.
The specific aims of this projects are to determine (a) the effect of ingesting Ginkgo biloba on the pharmacokinetics of glipizide, pioglitazone and metformin and (b) how the interaction between Ginkgo biloba and the three hypoglycemic agents affect the three homeostatic variables that control blood glucose levels: insulin synthesis, insulin action and hepatic glucose production. Because aging is a significant risk factor for the development of NIDDM as a result of a progressive decline in pancreatic function, and because the elderly chronically take multiple prescription medications, the increased use of Ginkgo biloba in this population may increase drug-herb interactions. Therefore, we shall examine the effect of Ginkgo biloba on the pancreatic function in the elderly to determine whether it may produce pancreatic dysfunction and a potential for the development of insulinopenia. The results of this study, when taken together should provide very important information on balancing the risk of accelerating pancreatic beta-cell dysfunction, with its beneficial effects on delaying the onset of cognitive function. The results of this study should also provide valuable information for designing new therapeutic strategies for the treatment of diseases in the insulin resistance syndrome.
