Objective:To investigate whether inflammation plays a role in accelerating glucose metabolism disorder in obese mice and whether the mechanism is regulated by liver gluconeogenesis. Methods:The C57BL/6J mice were randomly divided into normal chaw diet group

high fat diet group

high fat diet with chronic inflammation group（high fat diet with casein injection group）. The macrophage infiltration in the liver was detected by F4/80 staining. The m RNA relative expression levels of Mcp1

G-6-pase and Pepck were examined using real-time quantitative PCR. The liver glycogen content was detected qualitatively by Periodic acid-Schiff staining and quantitatively by anthrone-sulfuric acid method. The Fox O1 and Akt protein levels were analyzed by Western blot. Results :Casein injection induced obvious liver inflammation in high fat diet-fed mice（P=0.000）. The fasting blood glucose levels and the area under the insulin tolerance curve were higher in the casein-injected mice（P =0.040

P =0.025）. The liver glycogen content and the gluconeogenesis related gene G-6-pase and Pepck expression were also increased significantly（P=0.001

P=0.001）

while the phosphorylation of Akt and Fox O1 in the liver decreased obviously（P=0.021

P=0.003）after casein injection. High fat diet alone resulted in higher expression of gluconeogenesis genes（G-6-pase

Pepck）

while the blood glucose levels maintained in the normal range. Conclusion:Chronic inflammation can exacerbate glucose metabolism disorder in obese mice fed with high fat diet

resulting in hyperglycemia. It suggests that chronic inflammation may increase the risk of obese patients developing into type 2 diabetes

which provides clinical implications for the obese patients to prevent type 2 diabetes.