Objective: To elucidate the effect and mechanism of cinnamaldehyde (CA) in improving blood glucose in obese db/db mice. Method: Twenty-four 6 to 8-week-old male db/db mice were randomly divided into model group

Metformin group

low-dose CA group and high-dose CA group according to their levels of blood glucose

with 6 in each group

while six C57BL/6J mice of the same age were included in normal group. After treatment for four weeks

fasting blood glucose (FBG)

total cholesterd (TC)

total triglyceride (TG)

free fatty acids (FFA)

aspartate aminotransferase (AST)

fasting insulin (Fins)

homa insulin-resistance (HOMA-IR)

hepatic glycogen and PAS staining of liver were measured. Real-time PCR and Western blot were used to quantify the mRNA and protein expressions of certain targets in liver. Result: It was found that the body weight

fast blood glucose

Fins

HOMA-IR

lipid were significantly decreased in the CA group compared with model group after the treatment for 4 weeks (P<0.05

P<0.01). Hepatic glycogen was higher in the CA group than model group (P<0.01). The mRNA expressions of glucose-6-phosphate (G-6-P)

phosphoenolpyruvate carboxykinase (PEPCK) in mice of CA group decreased significantly (P<0.01)

and the protein expressions of p-protein kinase B (Akt)

p-glycogenkinase3β (GSK3β) in mice of CA group increased significantly (P<0.01). Conclusion: It was demonstrated that CA may reduce the blood glucose in db/db mice by up-regulating the mRNA expressions of G-6-P and PEPCK

and down-regulating the protein expressions of p-Akt

p-GSK3β in liver.