Abstract
BackgroundRecently, there has been increasing interest in Ficus deltoidea Jack. (Moraceae) due to its chemical composition and the potential health benefits. The present study was undertaken to investigate the effect of extracts of F. deltoidea leaves on diabetes.MethodsThe petroleum ether, chloroform and methanol extracts of F. deltoidea were prepared and subjected to standardization using preliminary phytochemical and HPLC analysis. Dose selection was made on the basis of acute oral toxicity study (50–5000 mg/kg b. w.) as per OECD guidelines. Diabetes mellitus was induced with streptozotocin and rats found diabetic were orally administered with the extract (250, 500 and 1000 mg/kg) for 14 days. Levels of blood glucose and insulin were measured in control as well as diabetic rats on 0, 7 and 14th day. In addition, glucose metabolism regulating gene expression was assessed using RT-PCR.ResultsHPLC analysis revealed that the methanol extract is enriched with C-glycosylflavones particularly, vitexin and isovitexin. In oral glucose tolerance test, oral administration of the methanol extract increased the glucose tolerance. The methanol extract showed significant (P < 0.01) antidiabetic activity. The extract treatment caused significant reduction (p < 0.01) in elevated fasting blood glucose level in streptozotocin-induced diabetic rats. The streptozotocin-related weight loss in rats was noticeably reversed by the extract treatment. Finally, RT-PCR analysis revealed a novel mechanisms for the anti-diabetic action of methanol extract of F. deltoidea. The extract exerted its effect via an increase of insulin secretion which impeded the hepatic glucose production, via down-regulation of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase genes expression on one hand, and up-regulation of hepatic GK and PPARγ genes expression on the other hand. The extract caused an increased expression of GLUT-4 gene expression in skeletal muscles which leads to normalize the hyperglycemia. The extract also nullified the toxic effects of streptozitocin by blocking its entry into the islet β-cells through reducing the expression of GLUT-2 gene.ConclusionIt can be concluded that, F. deltoidea could potentially inhibits the streptozitocin-induced hyperglycemia in rats. Further the herb can be utilized as useful remedy for alleviation of diabetes complications.
Highlights
There has been increasing interest in Ficus deltoidea Jack. (Moraceae) due to its chemical composition and the potential health benefits
The glucose transporter-4 (GLUT4) receptor is localized in intracellular vesicles, but when insulin binds to its own membrane receptor, GLUT4 is transported to the plasma membrane to permit glucose uptake into muscle cells
The rate of glycogenesis is due to the phosphorylase which is controlled by hormones whereas the rate of gluconeogenesis is controlled principally by the activities of unidirectional enzymes, such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (Glc-6-Pase)
Summary
There has been increasing interest in Ficus deltoidea Jack. (Moraceae) due to its chemical composition and the potential health benefits. Insulin is the key regulator of glucose uptake. The rate of glucose uptake into muscle cells is dependent on the action of insulin on the glucose transporter-4 (GLUT4) [2]. The GLUT4 receptor is localized in intracellular vesicles, but when insulin binds to its own membrane receptor, GLUT4 is transported to the plasma membrane to permit glucose uptake into muscle cells. The rate of glycogenesis is due to the phosphorylase which is controlled by hormones whereas the rate of gluconeogenesis is controlled principally by the activities of unidirectional enzymes, such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (Glc-6-Pase). The expression of PEPCK and GK the key enzymes of liver gluconeogenesis and glycolysis, is under the control of insulin [4]. Glucagon affects glucose metabolism mainly by inducing glycogen breakdown and glucose-6phosphatase on one hand whereas, on the other hand glucagon contributes the hyperglycemia by inhibiting the enzyme pyruvate kinase [6]
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