ABSTRACT
_ Objective_ To analyze the relationship between the fasting plasma glucose ( FPG ) of pre-pregnancy women and occurrence of gestational diabetes mellitus( GDM) , and to explore the value of risk evaluation of GDM by lowerling cut-point for impaired fasting glucose ( IFG ) . Methods The general clinic check information before pregnancy, the plasma glucose levels during 24-28 weeks of pregnancy and pregnancy outcomes were collected prospectively in Weifang and Zhucheng Maternal and Child Health Hospital between February 2014 and November 2014. The FPG levels of the recruited women were lower than 6. 1 mmol/L. According to the criteria for GDM of Ministry of Health (MOH)of China in 2011, and based on the results of 75 g oral glucose tolerance test, pregnant women who underwent screening for GDM were recruited and separated into normal group and GDM group. Based on the FPG levels before pregnancy and according to the recommendation as American Diabetes Association ( ADA ) suggested in 2003, recruited women with normal FPG level according to World Health Organization ( WHO) criteria (1999)were divided into 5. 6-6. 1 mmol/L and<5. 6 mmol/L groups. Results Among the child-bearing age women with FPG<6. 1 mmol/L, the incidences of GDM and macrosomia were 19. 2% and 8. 2% respectively. In the group with FPG between 5. 6 and 6. 1 mmol/L, incidences of GDM and macrosomia were 34. 2% and 4. 7%respectively. While in the group with FPG<5. 6 mmol/L, incidences of GDM and macrosomia were 13. 2% and 15. 3% respectively. The risks of GDM and macrosomia were increased by 2. 6 times and 3. 3 times respectively in group with FPG between 5. 6 and 6. 1 mmol/L (34. 5%), compared with that in group with FPG<5. 6 mmol/L(P<0. 01). Age, FPG, and body mass index before pregnancy in GDM group were significantly higher than those in normal group. The receiver operating characteristic curves in predicting GDM showed that the optimum cut-points for age, FPG, and body mass index were 30 years old, 5. 55 mmol/L, and 23. 7 kg/m2 respectively. Conclusions The risk of GDM in childbearing aged women with FPG from 5. 55 to 6. 10 mmol/L was markedly increased. The optimum cut-point for FPG (5. 55 mmol/L) in predicting GDM was close to the low limit for IFG (5. 6 mmol/L) suggested by ADA in 2003. Decreasing the lower limit of IFG to 5. 6 mmol/L among women who checked before pregnancy and paying attention to those women with FPG from 5. 6 to 6. 1 mmol/L would have advantage to the evaluation and prevention of GDM.
ABSTRACT
In order to investigate the effects of puerarin on pulmonary vascular remodeling and protein kinase C-alpha (PKC-alpha) in chronic exposure smoke rats, 54 male Wistar rats were randomly divided into 7 groups: control group (C group), smoke exposure groups (S(4w) group, S(8w) group), puerarin groups (P(4w) group, P(8w) group), propylene glycol control groups (PC(4w) group, PC(8w) group). Rats were exposed to cigarette smoke or air for 4 to 8 weeks. Rats in puerarin groups also received puerarin. To evaluate vascular remodeling, alpha-smooth muscle actin (alpha-SM-actin) staining was used to count the percentage of completely muscularised vessels to intraacinar pulmonary arteries (CMA/IAPA) which was determined by morphometric analysis of histological sections. Pulmonary artery smooth muscle cell (PASMC) apoptosis was detected by in situ end labeling technique (TUNEL), and proliferation by proliferating cell nuclear antigen (PCNA) staining. Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were done to detect the PKC-alpha mRNA and protein expression in pulmonary arteries. The results showed that in cigarette smoke-exposed rats the percentage of CMA/IAPA and alpha-SM-actin expression were increased greatly, PASMC apoptosis was increased and proliferation was markedly increased; Apoptosis indices (AI) and proliferation indices (PI) were higher than in C group; AI and PI were correlated with vascular remodeling indices; The expression of PKC-alpha mRNA and protein in pulmonary arteries was significantly higher than in C group. In rats treated with puerarin, the percentage of CMA/IAPA and cell proliferation was reduced, whereas PASMC apoptosis was increased; The expression levels of PKC-alpha mRNA and protein were lower than in smoke exposure rats. There was no difference among all these data between S groups and PC groups. These findings suggested that cigarette smoke-induced pulmonary vascular remodeling was most likely an effect of the imbalance of PASMC proliferation and apoptosis. Puerarin appears to be able to reduce cell proliferation and vascular remodeling possibly through PKC signaling transduction pathway.