Hypoglycemic effect of geniposide and its relative mechanism
10.7501/j.issn.0253-2670.2014.08.015
- Author:
Dong-Dong YAO
1
Author Information
1. College of Life Science, Anhui University
- Publication Type:Journal Article
- Keywords:
Diabetes;
Geniposide;
Glycogen synthase kinase;
Pancreatic β-cells;
Protein kinase B
- From:
Chinese Traditional and Herbal Drugs
2014;45(8):1121-1125
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the hypoglycemic effect of geniposide and to explore the mechanism. Methods: The diabetic mice were induced by a single dose of 90 mg/kg streptozotocin (STZ) injection followed by four-week high-fat diets and randomly divided into three groups: normal control (con), diabetic model (diab), and geniposide (gen, 100 mg/kg) groups. Body weight and fasting blood glucose were measured during the treatment. Thirty days later, the oral glucose tolerance test (OGTT) was performed, blood samples were collected to measure insulin concentration in plasma. The morphological changes of pancreas pathology and β-cell proliferation were examined by immuno-fluorescent staining of insulin and Ki67. The phosphorylations of AKT and GSK-3β (p-AKT and p-GSK-3β) in liver tissues were detected by Western blotting assay. Results: Compared with the diab group, geniposide showed significantly hypoglycemic effect, together with lowering body weight, increasing the insulin content in plasma, and improving OGTT. The immuno-fluorescent staining showed the islets destruction caused by hyperglycemia was recovered by geniposide. The β-cell proliferation presented by Ki67 staining increased as compared with that in the diab group. Moreover, both p-Akt and p-GSK-3β levels in the liver tissue were upregulated by geniposide remarkably. Conclusion: The present study demonstrates that geniposide could ameliorate the hyperglycemia in diabetic mice by enhancing the pancreatic β-cell proliferation and activation of AKT signaling pathway in liver.
