Antihyperglycemic and Antioxidant Properties of Jaceosidin, a Flavonoid Isolated from Artemisia Princeps, in Type 2 Diabetic Mice

Young-Jin Kang; Un-Ju Jung; Seon-Min Jeon; Ji-Young Yeo; Hye-Jin Kim; Dong-Ju Kim; Mi-Kyoung Lee; Nam-In Baek; Hae-Gon Chung; Myung-Sook Choi
June 2007
Diabetes;Jun2007 Supplement 1, Vol. 56, pA667
Academic Journal
Flavonoids have been identified as the antidiabetic components in a number of traditional ethnic remedies. However, the mechanisms whereby these compounds exert their hypoglycemic and antioxidant action in type 2 diabetes have rarely been investigated. Therefore, this study investigated the antidiabetic and antioxidant effects of jaceosidin (4',5,7-trihydroxy-3',6-dimethoxy flavone) isolated from Artemisia princeps using C57BL/KsJ-db/db mice. The db/db mice were divided into three groups; a diabetic control (DM), 0.005% Rosiglitazone (ROSI) and 0.02% jaceosidin (JACE). Rosiglitazone is an insulin sensitizer for the treatment of type 2 diabetes. ROSI and JACE supplement significantly lowered fasting blood glucose and HbA[sub 1c] levels compared to the DM group. In the intraperitoneal glucose and insulin tolerance test, JACE enhanced the glucose disposal and insulin sensitivity. The hepatic glycogen, plasma insulin and pancreatic insulin levels were higher in the JACE group than in the DM group. Immunohistochemistry of pancreas showed a substantial increase in the intensity of insulin staining in the islets of ROSI and JACE group. Supplementation of JACE significantly elevated hepatic glucokinase activities, whereas lowered hepatic phosphoenolpynivate carboxykinase activities. Erythrocytic superoxide dismutase(SOD), glutathione peroxidase(GSH-Px) and glutathione reductase(GR) activities were significantly higher in the ROSI and JACE group. And JACE supplement elevated hepatic SOD, catalase, GSH-Px and GR activities. Accordingly, these results suggest that JACE supplement exerts the antidiabetic properties in type 2 diabetic animals by improving the glucose and antioxidant metabolism and enhancing the pancreatic beta-cell function.


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