Black ginseng extract exerts anti-hyperglycemic effect via modulation of glucose metabolism in liver and muscle

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• 作者：Yun-Soo Seo^a ; ¹ ; Mi-Yae Shon^b ; ¹ ; Ryong Kong^a ; Ok-Hwa Kang^a ; Tian Zhou^a ; Do-Yeon Kim^b ; Dong-Yeul Kwon^a ; ^{sssimi@wku.ac.kr" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Black ginseng ; Diabetes mellitus ; Insulin signaling ; Glucose tolerance ; Skeletal muscle
• 刊名：Journal of Ethnopharmacology
• 出版年：2016
• 出版时间：22 August 2016
• 年：2016
• 卷：190
• 期：Complete
• 页码：231-240
• 全文大小：2126 K

文摘

Ginseng (Panax ginseng C. A. Meyer, Araliaceae) has been used as a traditional medicine for thousands of years for the treatment of a wide variety of diseases, including diabetes. Processed ginseng named Black ginseng exhibits more potent biological activities than white and red ginseng. The aim of this study was to investigate the effects of black ginseng extract (GBG05-FF) on hyperglycemia and glucose tolerance in streptozotocin (STZ)-induced diabetic mice.

Materials and methods

Black ginseng was produced by a repeated steaming and drying process, subsequent extraction with 70% ethanol, filtration, and lyophilization. The effect of GBG05-FF on glucose uptake and related protein expression and phosphorylation were determined in C2C12 cells. Furthermore, we evaluated the anti-diabetic effects of GBG05-FF in STZ-induced diabetic mice.

Results

GBG05-FF significantly (p<0.05) increased glucose uptake in C2C12 myotubes via AMPK, Sirt1 and PI3-K pathway. In addition, GBG05-FF improved the fasting blood glucose levels and glucose tolerance in STZ-induced diabetic mice. GBG05-FF decreased blood parameters such as glycated hemoglobin, triglyceride and total cholesterol. Quantitative RT-PCR assay revealed that in the STZ-induced diabetic mice treated with GBG05-FF, the expression of hepatic genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase (PEPCK), glucose 6-phosphatase (G6Pase)), glycogenolysis (liver glycogen phosphorylase (LGP)) and glycogenesis (glycogen synthase (GS)) was suppressed, while the expression of the genes involved in glucose uptake (glucose transporter (GLUT) 1, GLUT4) and β-oxidation (acyl-CoA oxidase (ACO), carnitine palmitoyl transferase 1a (CPT1a), mitochondrial medium chain acyl-CoA dehydrogenase (MCAD)) in muscle were increased. GBG05-FF delayed diabetes-associated muscle atrophy by activating mTOR. The major bioactive compounds including ginsenoside Rg1, Rg3(S), Rg3(R), Rg5, Rk1 and Rh4 were evaluated for glucose uptake effect in C2C12 myotubes; the data indicated that Rh4 significantly (p<0.05) increased glucose uptake.

Conclusion

Collectively, the results suggested that GBG05-FF is a potentially useful agent for treatment of diabetes by increasing glucose uptake.