Hypoglycemic mechanism of Cordyceps militaris aqueous extracts

• Main Authors: Cheng, Yu-Wen, 鄭裕文
• Other Authors: Lai, Yiu-Kay
• Format: Others
• Language: en_US
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/88326814955703460397

博士 === 國立清華大學 === 生物科技研究所 === 101 === There are many diabetic complications which induce patients’ disability or loss their life. Previous study found Cordyceps militaris (CM) had hypoglycemic effect, yet the actual mechanism remains unclear. We would like to explore the mechanism of CM’s hypoglycemia. The experiments were separated into two portions. In the first one, aqueous extracts of CM was feeding to the normal Wistar rats. The optimal dose of CM for lowering serum glucose was tested first and found that 10 mg/kg CM had a better hypoglycemic effect than a higher dose (100 mg/kg). Such optimal dose was used in following experiments. In the normal rats, CM decreased plasma glucose by 21.0% and induced additional insulin secretion by 54.5% at 30 minute. Additionally, atropine 0.1 mg/kg was injected intraperitoneally as an antagonist to the cholinergic nerve. The hypoglycemic effects of CM vanished and the enhanced insulin secretion was also blocked. In the assay of insulin signaling proteins, a significant rise in the insulin receptor substrate 1 (IRS-1) and glucose transporter 4 (GLUT-4) were found in the rats after being fed CM (3.63- and 2.64-fold in comparison with fed saline). However, these rising signaling proteins were blocked by the atropine. And the same responses were found in the hemicholinium-3 (5μg/kg intraperitoneally) pre-treated rats. The second portion of experiments was performed to the streptozotocin (STZ)- induced diabetic rats. Blood glucose decreased 7.2% in the CM group but only 1.5% in the control group. The IRS-1 signal was 2.9-fold in the CM group but only 0.8-fold in the control group. In GLUT-4 signal, it was 1.7- vs. 0.6-fold, respectively. However, atropine injection made CM-induced hypoglycemia or elevation of IRS-1 and GLUT-4 not significant. In conclusion, CM stimulates the pancreas of normal rats to secrete additional insulin and activates the insulin signaling proteins via the binding of more insulin to its receptors in the myocyte. In the STZ-induced diabetic rats, the influence of insulin hypoglycemic effect was little, but CM still had the effect of activating insulin signaling proteins in the myocytes. Both reactions were blocked by anti-cholinergic agents. Taken together, the possible mechanisms of CM-induced hypoglycemia in both types of animal models were the induction of insulin secretion and non-insulin dependent hypoglycemic effect mainly triggered by activation of the cholinergic nerve.