ObjectiveThe relationship between gestational diabetes mellitus (GDM) and oxidative stress has not been fully elucidated. This study examined the association between biomarkers of oxidative stress and GDM.MethodsWe conducted a case-control study which included 36 women presenting with GDM and 36 asymptomatic matched control subjects who visited Guangzhou Women and Children’s Medical Centre, China, from June 2012 to December 2012. Pregnant women were prospectively recruited to the study, and blood samples were collected at the time of a routine oral glucose tolerance test. These samples were then analyzed for levels of endocrine and surrogate markers of oxidative stress.ResultsCompared to control subjects, women with GDM exhibited elevated values for plasma glucose, insulin, and insulin resistance (IR), and showed reduced HOMA pancreatic β-cell function (HOMA-B), insulin sensitivity index (ISI), insulinogenic index, and corrected insulin response at 24–28 weeks gestation. A bivariate logistic regression analysis showed that levels of high-sensitivity C reactive protein (hs-CRP) and high fluorescence reticulocytes at fasting, and hs-CRP in a 1-h OGTT, were significantly associated with GDM. A linear regression analysis showed that levels of hs-CRP (P = 0.003) and reticulocytes (P = 0.029) at fasting were associated with IR, and levels of hs-CRP (P = 0.002) and monocytes (P = 0.006) in a 1-h OGTT were associated with ISI.ConclusionsPregnant women with GDM developed a pathological IR and exhibited β-cell dysfunction. Their decreased ability to compensate for oxidative stress was associated with increased IR and a reduced ISI, which might be important factors in GDM.

The woman’s gut microbiota during pregnancy may support nutrient acquisition, is associated with diseases, and has been linked to infant health. However, there is limited information on gut microbial characteristics and dependence in pregnant women. In this study, we provide a comprehensive overview of the gut microbial characteristics of 1479 pregnant women using 16S rRNA gene sequencing of fecal samples. We identify a core microbiota of pregnant women, which displays a similar overall structure to that of age-matched nonpregnant women. Our data show that the gestational age-associated variation in the gut microbiota, from the ninth week of gestation to antepartum, is relatively limited. Building upon rich metadata, we reveal a set of exogenous and intrinsic host factors that are highly correlated with the variation in gut microbial community composition and function. These microbiota covariates are concentrated in basic host properties (e.g., age and residency status) and blood clinical parameters, suggesting that individual heterogeneity is the major force shaping the gut microbiome during pregnancy. Moreover, we identify microbial and functional markers that are associated with age, pre-pregnancy body mass index, residency status, and pre-pregnancy and gestational diseases. The gut microbiota during pregnancy is also different between women with high or low gestational weight gain. Our study demonstrates the structure, gestational age-associated variation, and associations with host factors of the gut microbiota during pregnancy and strengthens the understanding of microbe–host interactions. The results from this study offer new materials and prospects for gut microbiome research in clinical and diagnostic fields.

Maternal WBC, RBC, and PLT counts are important correlates of GDM. Increased volume of RBC and PLT might protect pregnant women from development of GDM.

Epidemiologic studies showed that low birth weight is associated with high cholesterol and an increased risk of cardiovascular diseases in adulthood. This study aimed to elucidate the intrauterine programming mechanisms of adult hypercholesterolemia. The results showed that prenatal nicotine exposure (PNE) caused intrauterine growth retardation and hypercholesterolemia in male adult offspring rats. Hepatic cholesterol synthesis and output were deceased in utero but increased in adults; hepatic reverse cholesterol transport (RCT) persistently deceased before and after birth. Meanwhile, PNE elevated serum corticosterone level and decreased hepatic IGF1 pathway activity in male fetuses, whereas converse changes were observed in male adults. The chronic stress model and cortisol-treated HepG2 cells verified that excessive glucocorticoid (GC)-induced GC-IGF1 axis programming enhanced hepatic cholesterol synthesis and output. In addition, PNE decreased the expression of specific protein 1 and P300 enrichment and H3K27 acetylation at the promoter region of genes responsible for RCT both in fetal and adult, male livers and reduced expression of those genes, similar alterations were also confirmed in cortisol-treated HepG2 cells, suggesting that excessive GC-related programming induced continuous RCT reduction by epigenetic modification. Taken together, the "2-programming" approach discussed above may ultimately contribute to the development of hypercholesterolemia in male adult offspring.-Zhou, J., Zhu, C., Luo, H., Shen, L., Gong, J., Wu, Y., Magdalou, J., Chen, L., Guo, Y., Wang, H. Two intrauterine programming mechanisms of adult hypercholesterolemia induced by prenatal nicotine exposure in male offspring rats.

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