Objective To analyze the effect and possible mechanism of Jianpi Xiaoke Formula（ JPXKF） on type 2 diabetes mellitus（ T2DM） rats. Methods Totally 46 rats were randomly assigned to normal group（ n =10） and model-making group（ n = 36）. The normal group was given regular forage

while the model group was fed with high-glucose and high-fat forage. After 6 weeks

the model-making group were intraperitoneally injected with streptozotocin（ 30 mg / kg） to make T2 MD models

and the 36 successfully made models rats were randomly divided to Model group

Glibenclamide group

TCM group

with 12 rats in each. The Glibenclamide group and TCM group were given glibenclamide suspension 0. 27 mg /（ kg·d） and JPXKF decoction 6. 36 g /（ kg·d） by gavage respectively

while the normal group and Model group were given the same amount of normal saline. After six weeks

all rats were weighed and fasting blood glucose（ FBG）

fasting insulin（ FINS）

glucagon（ GC） were tested. Insulin resistance index（ HOMA-IR） and insulin secretion index（ HOMA-β） were calculated. Immunofluorescence was used to analyze the distribution and localization of islet β / α cells in the pancreas. Results The FGB and weight of the Glibenclamide group and TCM group were significantly decreased after treatment

and decrease of FBG at the same time was more significant compared with the Model group（ P < 0. 05 or P < 0. 01）. Compared with the Model group

the GC levels of the Glibenclamide group and TCM group were significantly lower（ P < 0. 01）

while FINS

HOMA-β levels were significantly higher（ P < 0. 05 or P < 0. 01）. The FINS

HOMA-IR

HOMA-β levels of the Glibenclamide group were significantly higher than those of the TCM group（ P < 0. 05）. Immunofluorescence test showed that the number of islet β cells in the TCM group were significantly more while the number of islet α cells was reduced than that of the Model group and Glibenclamide group. Conclusion JPXKF could increase FINS

decrease GC

reduce insulin resistance and regulate the distribution and number of islet α

β cells in T2 DM rat

which may be one of the mechanisms.