期刊
ENDOCRINE JOURNAL
卷 58, 期 9, 页码 761-768出版社
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.K11E-024
关键词
Diabetic mouse; Berberine; Akt signaling pathway; GSK-3 beta; Glucokinase
资金
- National Natural Science Foundation of China [30873427]
- Science and Technology Program of Guangdong province, PR China [2008B030301117]
- Key Project of Guangdong/Hong Kong Critical Technology Field, PR China [2008A030600008]
Recently, it is implicated that the abnormality of Akt signaling pathway is involved in the diabetic pathology. Previous studies have demonstrated that berberine could decrease blood glucose by elevating liver glycogen synthesis. However, the underlying mechanism is still unclear. In the present study, we investigated the effects of berberine on fasting blood glucose, liver glycogen, Akt, Glycogen synthase kinase-3, glucokinase and insulin receptor substrate (IRS) in alloxan-induced diabetic mice, exploring its possible hypoglycemic mechanism. We found that in alloxan-induced diabetic mice, the high blood glucose was significantly lowered by berberine treatment. Liver glycogen content, the expression and activity of glucokinase and the phosphorylated Akt and IRS were all significantly reduced in diabetic mice whereas berberine blocked these changes. Berberine also depressed the increasing of phosphorylated GSK-3 beta in diabetic mice. Collectively, Berberine upregulates the activity of Akt possibly via insulin signaling pathway, eventually lowering high blood glucose in alloxan-induced diabetic mice.
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