title: Ginkgo biloba extract enhances glucose tolerance in hyperinsulinism-induced hepatic cells.
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.
authors.affiliation: Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of the Ministry of Education, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, Hubei, People's Republic of China. zhoulei@mail.hzau.edu.cn
authors.forename: Lei
authors.initials: L
authors.lastname: Zhou
authors.forename: Qingjie
authors.initials: Q
authors.lastname: Meng
authors.forename: Tao
authors.initials: T
authors.lastname: Qian
authors.forename: Zaiqing
authors.initials: Z
authors.lastname: Yang
mesh_terms: D002460:Cell Line; D020441:Ginkgo biloba / Q000737:chemistry*; D005941:Glucokinase / Q000235:genetics; D005947:Glucose / Q000378:metabolism*; D005952:Glucose-6-Phosphatase / Q000235:genetics; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism*; D006801:Humans; D006946:Hyperinsulinism / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics; D010936:Plant Extracts / Q000737:chemistry* / Q000494:pharmacology*; D012333:RNA, Messenger; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology
chemical_list: C526297:IRS2 protein, human; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D047495:PPAR gamma; D010936:Plant Extracts; D012333:RNA, Messenger; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D005941:Glucokinase; D005952:Glucose-6-Phosphatase; D005947:Glucose
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