Expression of Akt and GLUT-4 in adipose tissue of women with gestational diabetes mellitus and pregnant women with excessive weight gain / 解放军医学杂志

ABSTRACT

 Objective To investigate the influence of glucose transporter 4 (GLUT-4) and protein kinase B (Akt) on gestational diabetes mellitus (GDM) by determining their expressions in adipose tissues from women with GDM, excessive weight gain pregnant women, and normal pregnant women. Methods Adipose tissues were obtained by biopsy during cesarean section from 15 pregnant women with normal glucose tolerance while their body mass index (BMI) increased in about 4kg/m (NG 2group), and 15 pregnant women with normal glucose tolerance with BMI increased by 8kg/m (NGT2 group), and 15 cases of GDM (GDM group). Adipose tissue were divided into two sections and incubated in the culture medium with or without insulin (1 X 10 mol/L) for 30 minutes. Fasting blood glucose (FBG) and fasting insulin (FINS) levels were determined with glucose oxidase and radioimmunoassay. Homeostatic model assessment of insulin resistance (HOMA-IR), and homeostatic model assessment of insulin secretions index (HOMA-IS) were calculated from the data. Phosphorylation of Akt (P-Akt) and GLUT-4 levels of cultured adipose tissue were examined by Western blotting. Results The FBG levels were similar in 3 groups. FINS, HOMA-IR and HOMA-IS were significantly different among the 3 groups (P0.05) in basal state. Compared with the basal state, however, the phosphorylation of Akt increased significantly in NGT1 group (P0.05) after insulin stimulation. The expression of GLUT-4 was significantly lower in GDM group and NGT2 group than in NGT1 group (P<0.05) in basal state. The expression of GLUT-4 increased much more in NGT1 group than in NGT2 group or GDM group (P<0.05) after insulin stimulation. Conclusion The excessive weight gain and normal glucose tolerance pregnant women almost share a similar expression with GDM women in the insulin signaling and glucose transporter proteins, Akt and GLUT-4, and their abnormal expression and function might play an important role in insulin resistance and GDM morbidity.