The objective was to investigate the
hypoglycemic action of
catalpol in spontaneous diabetes db/db mice. 40 db/db mice were randomly divided into fi ve groups: model control gourp; db/db plus
catalpol 40, 80, 120 mg/kg body wt. groups and db/db plus
metformin 250 mg/kg group. Age-matched db/m mice were selected as normal control group. The mice were administered with corresponding drugs or
solvent by gavage for 4 weeks. The oral
glucose tolerance test was carried out at the end of 3(rd) week. After 4 weeks of treatment, the concentrations of fasting
blood glucose (FBG),
glycated serum protein (GSP),
insulin (INS),
triglyceride (TG), total
cholesterol (TC) and adiponection (APN) in serum were detected. The
protein expressions of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and
glucose transporter-4 (GLUT-4) in skeletal muscle and adipose tissues were detected by western blot. Real time RT-PCR was used to detect the
mRNA expressions of
acetyl-CoA carboxylase (ACC) and Hydroxymethyl
glutaric acid acyl CoA reductase (HMGCR) in liver. Our results showed that
catalpol could significantly improve the
insulin resistance, decrease the serum concentrations of INS, GSP, TG, and TC. The concentrations of APN in serum, the
protein expression of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and GLUT-4 in peripheral tissue were increased.
Catalpol could also down regulate the
mRNA expressions of ACC and HMGCR in liver. In conclusion,
catalpol ameliorates diabetes in db/db mice. It has benefi t eff ects against
lipid/
glucose metabolism disorder and
insulin resistance. The mechanism may be related to up-regulating the expression of phosphorylation-AMPKα1/2.