Introduction Gestational diabetes mellitus (GDM) is usually a metabolic disorder during mid- to late-pregnancy characterized by hyperglycemia, insulin resistance and fetal mal-development. glucose tolerance test (IPGTT). In addition, levels of GLUT2 and SGLT2 were evaluated to further explore the underlying mechanism of GDM. Results HFD feeding induced abnormal glucose rate of metabolism as manifested by improved levels of blood glucose and insulin and prominent glucose intolerance. Additionally, fetal mice from mother feed on HFD showed higher mean body weight. Furthermore, HFD feeding led to an increase in the number of positive cells of GLUT2 and SGLT2 in the renal proximal tubule and the expressions of renal GLUT2 and SGLT2 mRNA and proteins in mice. However, no obvious switch was observed in renal morphology. Summary Our study demonstrates a potential involvement of renal GLUT2 and SGLT2 in GDM pathology in an HFD-induced GDM mouse model, which further helps the part of renal GLUT2 and SGLT2 not only in T1DM and T2DM but also in GDM. = 30 per group): control or HFD group. Mice consumed control rodent diet (10% kcal excess fat; Research Diet programs, New Brunswick, NJ) or HFD (45% kcal excess fat; Research Diet programs, New Brunswick, NJ) (Table 1). After 6-week diet intervention, mice in control group were divided into two subgroups (= 15): control virgin group (CV) and control pregnant group (CP), and mice in HFD group were divided into HFD virgin group (HV) and HFD pregnant group (HP) (= 15). Woman mice in CP and HP organizations were mated with males of the same genotype inside a ratio of 1 1:2. The Mouse monoclonal to UBE1L next morning, female rats were observed for the presence or absence of vaginal suppositories, which were taken having a cotton swab and observed further under the microscope. If sperms were found in three different fields, the female rate was designated as positive for pregnancy, and the day was designated as gestation day time (GD) 0. The mating process lasted for 1 week which comprised approximately one estrous cycle. Non-pregnant female mice in this period were regarded as infertile and excluded from the study. Luckily, all 30 female rates were found pregnant. Then, the mice in HV and HP organizations continued feeding HFD until GV-58 GD 18. Table 1 Method And Nutrient Of Normal And High-Fat Diet programs (GAPDH) (ahead: CCCTCTGGAAAGCTGTGG 5-3, reverse: AGTGGATGCAGGGATGATG 5-3). Relative changes in gene manifestation were determined using the 2 2?ct method, with the housekeeping gene GAPDH as an internal control. Statistical Analysis All data were calculated as means SD and checked using the KolmogorovCSmirnov (KS) test before further analysis. Statistical significance between two datasets was assessed using the Students value of <0. 05 was considered statistically significant. All statistical tests were performed using GraphPad Prism Version 6.0 (GraphPad Prism Software, Inc. CA, USA). Results Changes Of Body Weight, Blood Glucose, And Serum Insulin In Mice GV-58 GV-58 Body weight was determined at different time points for GV-58 all groups. As indicated in Figure 1A, the body weight showed an increasing trend after 6 weeks of HFD, and a rapid elevation of body weight was found in the mice of HP group compared to the moderate increase in CP group (P <0.05). The weight at GD 18 and total weight gain of mice in HV and HP groups were significantly higher than that of CV and CP groups (P <0.05, Figure 1B). Next, we examined GV-58 the blood glucose and serum insulin in these mice. Blood glucose levels exhibited a gradual upregulation at the end of 6-week HFD feeding and during pregnancy in the mice of HV and HP groups but not CV or CP group (P <0.05, Figure 1C). Similar to the trend of blood glucose change, serum insulin levels were enhanced at the end of HFD feeding.