Abstract:

BACKGROUND: Studies found that fetal growth restriction can lead to adaptive change of metabolism and redintegration of hormones system, result in child development delay and insulin resistance after grow up. However, the molecule mechanism of the variation during pathological process from fetal growth restriction to insulin resistance remains poorly understood. 
OBJECTIVE: To explore the potential molecule mechanism of fetal growth restriction to insulin resistance, and to provide basis for the early diagnosis and intervention on metabolic disease.
METHODS: SD rats were randomly divided into the fetal growth restriction group and normal control group. Rats in the former group were prepared for fetal growth restriction models. The placenta protein was extracted from each group, and the protein kinase activity and inhibitor on MAP kinase (MAPK) signaling pathway were analyzed by plication of specific anti-phosphorylation antibody immunoprecipitation and Western blot.
RESULTS AND CONCLUSION: MAPK signal transduction pathway of ERK1/2, SAPK/JNK and Raf-1 protein kinase activity of the fetal growth restriction group were obviously decreased than those of the normal control group (P < 0.05), but the p38MAPK, MAP Kinase Kinases protein kinase activity in two groups did not change significantly (P > 0.05). In contrast, MAPK signal transduction pathway inhibitors in the fetal growth restriction group were higher than that of the normal control group (P < 0.05). The incidence of fetal growth restriction is closely related to abnormal MAP kinase signal transduction and apoptosis mechanism.