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.
Highlights
Obesity has become a major public health problem worldwide [1,2]
The aim of the present study was to evaluate the effect of Ginkgo biloba extract (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
The high-fat diet (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)
Summary
It has been suggested that high levels of abdominal adiposity and excess saturated fat intake promote obesity-related metabolic syndrome [3,4,5], and that the association between obesity, insulin resistance, and dyslipidemia potentiates the risk for cardiovascular diseases [6]. Ginkgo biloba extract (GbE; a standardized preparation named EGb 761, which is obtained from the leaves of G. biloba) is one of the plant extracts most used in therapeutics [7]. Antioxidant, anti-inflammatory, vasodilator, and anti-edematogenic properties have been reported for this plant [9,10]. Studies have suggested that GbE intake by type 2 diabetes mellitus (T2DM) patients reduces circulatory diseases and improves the glycemic profile [11,12]. Reduced glycemia was reported in streptozotocininduced diabetic rats [13]. It has been suggested that these beneficial effects could result from a significant stimulation of pancreatic beta-cell function/insulin production [11] and from a significant decrease in glycated
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