title: Beneficial effects of Ginkgo biloba extract on insulin signaling cascade, dyslipidemia, and body adiposity of diet-induced obese rats.
abstract: Ginkgo biloba extract (GbE) has been indicated as an efficient medicine for the treatment of diabetes mellitus type 2. It remains unclear if its effects are due to an improvement of the insulin signaling cascade, especially in obese subjects. The aim of the present study was to evaluate the effect of GbE on insulin tolerance, food intake, body adiposity, lipid profile, fasting insulin, and muscle levels of insulin receptor substrate 1 (IRS-1), protein tyrosine phosphatase 1B (PTP-1B), and protein kinase B (Akt), as well as Akt phosphorylation, in diet-induced obese rats. Rats were fed with a high-fat diet (HFD) or a normal fat diet (NFD) for 8 weeks. After that, the HFD group was divided into two groups: rats gavaged with a saline vehicle (HFD+V), and rats gavaged with 500 mg/kg of GbE diluted in the saline vehicle (HFD+Gb). NFD rats were gavaged with the saline vehicle only. At the end of the treatment, the rats were anesthetized, insulin was injected into the portal vein, and after 90s, the gastrocnemius muscle was removed. The quantification of IRS-1, Akt, and Akt phosphorylation was performed using Western blotting. Serum levels of fasting insulin and glucose, triacylglycerols and total cholesterol, and LDL and HDL fractions were measured. An insulin tolerance test was also performed. Ingestion of a hyperlipidic diet promoted loss of insulin sensitivity and also resulted in a significant increase in body adiposity, plasma triacylglycerol, and glucose levels. In addition, GbE treatment significantly reduced food intake and body adiposity while it protected against hyperglycemia and dyslipidemia in diet-induced obesity rats. It also enhanced insulin sensitivity in comparison to HFD+V rats, while it restored insulin-induced Akt phosphorylation, increased IRS-1, and reduced PTP-1B levels in gastrocnemius muscle. The present findings suggest that G. biloba might be efficient in preventing and treating obesity-induced insulin signaling impairment.
authors: Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, SP, Brasil.
authors: R M
authors: RM
authors: Banin
authors: Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, SP, Brasil.
authors: B K S
authors: BK
authors: Hirata
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: I S
authors: IS
authors: Andrade
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: J C S
authors: JC
authors: Zemdegs
authors: Faculdade de Nutrição, Universidade Federal de Alagoas, Maceió, AL, Brasil.
authors: A P G
authors: AP
authors: Clemente
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: A P S
authors: AP
authors: Dornellas
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: V T
authors: VT
authors: Boldarine
authors: Departamento de Biociências, Universidade Federal de São Paulo, Baixada Santista, SP, Brasil.
authors: D
authors: D
authors: Estadella
authors: Curso de Nutrição, Universidade Federal do Rio de Janeiro, Macaé, RJ, Brasil.
authors: K T
authors: KT
authors: Albuquerque
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: L M
authors: LM
authors: Oyama
authors: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
authors: E B
authors: EB
authors: Ribeiro
authors: Departamento de Ciências Biológicas, Universidade Federal de São Paulo, Diadema, SP, Brasil.
authors: M M
authors: MM
authors: Telles
mesh_terms: D050154:Adiposity / Q000187:drug effects*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects; D050171:Dyslipidemias / Q000188:drug therapy* / Q000378:metabolism; D004435:Eating / Q000187:drug effects; D020441:Ginkgo biloba / Q000737:chemistry*; D005951:Glucose Tolerance Test; D007003:Hypoglycemia / Q000097:blood; D007328:Insulin / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins / Q000032:analysis; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000737:chemistry; D009765:Obesity / Q000188:drug therapy* / Q000209:etiology; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1 / Q000032:analysis; D051057:Proto-Oncogene Proteins c-akt / Q000032:analysis; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D010936:Plant Extracts; D014280:Triglycerides; D051057:Proto-Oncogene Proteins c-akt; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1