Objective      To determine the effect and investigate the mechanism of bone morphogenetic protein 7（BMP7）on glucose metabolism in type 2 diabetic mice.  Methods         C57BL/6 mice (male

8 weeks old) were used for the establishment of type 2 diabetic mouse model by lowdose streptozocin injection combined with highfat chow. The type 2 diabetic mice were divided into 4 groups（n=20）：type 2 diabetic mice model group

PBS control group(i.p.

injected with phosphate buffered solution)

low-dose BMP7 group (100 μg/kg

i.p.injection every other day)and highdose BMP7 group (200 μg/kg

i.p.injection every other day）. Four weeks later

blood glucose

total blood cholesterol

triglyceride

serum insulin and body weight were measured. The insulin secretion index homeostasis model assessment of β-cell (HOMA-β) and insulin resistance index HOMA-IR were calculated. Finally

the mice’s pancreas were resected

and the protein expression and phosphorylation level of protein kinase D1（PKD1）were detected by Western blotting. Results      Compared with the model group and PBS control group

the blood glucose and triglyceride were significantly decreased

and the insulin level and HOMA-β index were significantly increased in both lowdose and highdose BMP7 groups（P0.05）. BMP7 treatment resulted in significant reduction of body weight compared with the control group（P0.05）. The HONMA-IR was lower in high-dose BMP7 group than in the control group（P0.05）. Western blot analysis showed that the expression of total PKD1 was not obviously changed by BMP7 treatment（P0.05）

but the phosphorylation of PKD1 was greatly increased in both BMP7 groups compared with the control（P0..05）. Conclusion        BMP7 improves glucose metabolism through enhancing insulin secretion and attenuating insulin resistance. Its effect on insulin secretion may be associated with increased phosphorylation of PKD1.