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Ginkgo biloba extract enhances glucose tolerance in hyperinsulinism-induced hepatic cells

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Abstract

Ginkgo biloba, an herbal medication, is capable of lowering glucose, fat, and lipid peroxide in diabetic patients. In the current study, we tested the hypothesis that Ginkgo biloba extract (GBE) prevented hyperinsulinism-induced glucose intolerance in hepatocytes. We investigated the effects of GBE on glucose consumption, glucokinase activity, and mRNA levels of key genes in glucose metabolism and the insulin signaling pathway. To better show its efficacy, we included a control group that was treated with rosiglitazone, a type of thiazolidinedione (TZD). The data indicated that GBE repressed glucose uptake under normal conditions, while it dramatically improved glucose tolerance under insulin-resistant conditions. Furthermore, after analyzing gene expression, we suggest that GBE chiefly exerts its effects by stimulating IRS-2 transcription. It should be noted that, unlike rosiglitazone, GBE did not stimulate excessive glucose uptake as it improved glucose tolerance. It is said that GBE treatment could avoid drug-induced obesity. Our data suggest that GBE has the potential to prevent insulin resistance and is a promising anti-diabetic drug.

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Abbreviations

GBE:

Ginkgo biloba extract

G6Pase:

Glucose-6-phosphatase

IRS:

Insulin receptor substrate

GLUT:

Glucose transporter

PPAR:

Peroxisome proliferator-activated receptor

SREBP:

Sterol regulatory element-binding protein

TZD:

Thiazolidinedione

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Acknowledgments

This work was supported by grants from Major Projects of National Science and Technology (2009ZX08009-151B), 973 Program (2006CB102100), 863 Program (2008AA10Z134), China National Fundamental Fund of Personnel Training (J0730649), Program of National Natural Science Foundation of China (30771585, 30970356), and the Fundamental Research Funds for the Central Universities (2009BQ046).

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Correspondence to Zaiqing Yang.

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Zhou, L., Meng, Q., Qian, T. et al. Ginkgo biloba extract enhances glucose tolerance in hyperinsulinism-induced hepatic cells. J Nat Med 65, 50–56 (2011). https://doi.org/10.1007/s11418-010-0456-z

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  • DOI: https://doi.org/10.1007/s11418-010-0456-z

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