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Anti-Diabetic Effect of Pectinase-Processed Ginseng Radix (GINST) in High Fat Diet-Fed ICR Mice

In the present study, we investigate anti-diabetic effect of pectinase-processed ginseng radix (GINST) in high fat diet-fed ICR mice. The ICR mice were divided into three groups: regular diet group, high fat diet control group (HFD), and GINST-treated group. To induce hyperglycemia, mice were fed a...

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Detalles Bibliográficos
Autores principales: Yuan, Hai Dan, Quan, Hai Yan, Jung, Mi Song, Kim, Su Jung, Huang, Bo, Kim, Do Yeon, Chung, Sung Hyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Ginseng 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659543/
https://www.ncbi.nlm.nih.gov/pubmed/23717074
http://dx.doi.org/10.5142/jgr.2011.35.3.308
Descripción
Sumario:In the present study, we investigate anti-diabetic effect of pectinase-processed ginseng radix (GINST) in high fat diet-fed ICR mice. The ICR mice were divided into three groups: regular diet group, high fat diet control group (HFD), and GINST-treated group. To induce hyperglycemia, mice were fed a high fat diet for 10 weeks, and mice were administered with 300 mg/ kg of GINST once a day for 5 weeks. Oral glucose tolerance test revealed that GINST improved glucose tolerance after glucose challenge. Compared to the HFD control group, fasting blood glucose and insulin levels were decreased by 57.8% (p<0.05) and 30.9% (p<0.01) in GINST-treated group, respectively. With decreased plasma glucose and insulin levels, the insulin resistance index of the GINST-treated group was reduced by 68.1% (p<0.01) compared to the HFD control group. Pancreas of GINST-treated mice preserved a morphological integrity of islets and consequently having more insulin contents. In addition, GINST up-regulated the levels of phosphorylated AMP-activated protein kinase (AMPK) and its target molecule, glucose transporter 4 (GLUT4) protein expression in the skeletal muscle. Our results suggest that GINST ameliorates a hyperglycemia through activation of AMPK/ GLUT4 signaling pathway, and has a therapeutic potential for type 2 diabetes.