[Associations of Pre-pregnancy Body Mass Index and Gestational Weight Gain with Gestational Diabetes Mellitus: a Cohort Study in Southwest China].

OBJECTIVE: To determine the associations of pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) with gestational diabetes mellitus (GDM). METHODS: A prospective cohort of pregnant women were screened for GDM at 24-28 weeks of gestation between 2013 and 2015, resulting in a sample of 3 593 with GDM and 15 346 without GDM. The body mass, plasma glucose, and height data of the participants were collected by the local medical workers. Multivariate logistic regression analyses were performed to determine the associations of pre pregnancy body mass index and weight gain during pregnancy with GDM. RESULTS: The participants with pre pregnancy overweight [odds ratio(OR)=2.44, 95% cofidence interval(CI)1.98-2.99] and obesity (OR=4.98, 95%CI 2.52-9.91) were more likely to develop GDM. According to the Institute of Medicine (IOM) criteria, excessive GWG in the first trimester occurred in 8.46% of the women, compared with 55.07% in the second trimester. After adjustment for age at delivery and pre pregnancy BMI, high GWG in the first trimesters in advanced maternal age (age at delivery≥35 yr.) group (OR=1.42, 95%CI 1.02-2.28) was a risk factor for GDM while the OR value of the non-advanced maternal age (age at delivery≤35 yr.) group was not statistically significant. In second trimesters, both advanced maternal age group (OR=1.59, 95%CI 1.14-1.88) and non-advanced maternal age group (OR=1.49, 95%CI 1.20-1.72) in high GWG were associated with high risk of GDM. CONCLUSION: Pre pregnancy overweight and obesity and excessive GWG during early and second trimesters of pregnancy may increase the risk of GDM in women in Southwestern China.

Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. In this study, we investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats. RESULTS: GLA treatment at dose of 30 mg/kg decreased LPS-induced lung W/D ratio and alleviated evident lung histopathological changes. Expressions of TNF-α and IL-18 were suppressed by GLA in plasma. The levels of SPA, MDA and NO in lung were down-regulated significantly in groups administrated with GLA. While the SOD level increased after GLA administration. Additionally, the attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPS-induced ARDS rats. MATERIALS AND METHODS: Sixty-four Wistar rats were randomly assigned into control group, Glabridin (GLA) alone group, LPS groups (6 h, 12 h, 24 h), GLA with LPS groups (6 h, 12 h, 24 h). ARDS was induced in rats by intraperitoneal administration of LPS (10 mg/kg). The degree of lung edema was evaluated by calculating the wet/dry weight ratio. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin-18 (IL-18) were assayed by enzyme-linked immunosorbent assay (ELISA). Surfactant protein A (SPA), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were analyzed. Pathological changes of lung tissues were observed by H&E staining. The protein expression of p38MAPK and ERK was detected using immunohistochemical techniques. Lung phosphorylated p38MAPK (p-p38MAPK) and pERK protein expression changes were detected by Western blotting. CONCLUSIONS: Glabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation.