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  • 1
    In: Gene, Elsevier BV, Vol. 533, No. 2 ( 2014-01), p. 481-487
    Type of Medium: Online Resource
    ISSN: 0378-1119
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 1491012-3
    SSG: 12
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  • 2
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 43, No. 4 ( 2017), p. 1526-1532
    Abstract: Background/Aims: Vitamin D deficiency has been shown to be associated with a greater prevalence of anemia in various healthy and diseased populations by a great deal of observational studies. However, less work has been done to explore this association in pregnant women. The aim of this study was to evaluate the association between maternal serum 25-hydroxyvitamin D [25(OH)D] concentrations and risk of gestational anemia in a large, nested case-control study. Methods: The serum 25(OH)D concentrations was measured by enzyme immunoassay in 775 pregnant women affected with anemia and 1550 controls. Logistic regression analysis was conducted to assess the association of 25(OH)D concentrations with risk of gestational anemia. Results: We found the 25(OH)D concentrations was significantly lower in women affected with anemia than in controls. Logistic regression analyses showed that women with 25(OH)D concentrations 〈 25.0 nmol/L, from 25.0 to 37.4 nmol/L and from 37.5 to 49.9 nmol/L all had increased risk of anemia when compared with women with concentrations from 50.0 to 74.9 nmol/L. And the risk of anemia was significantly increased with the decreasing concentrations of the serum 25(OH)D in a dose-dependent manner (P for trend = 0.012). For women with concentrations 〈 50.0 nmol/L, they had an 80% increase in anemia risk (95% CI = 1.45-2.25) after adjustment for confounders. We also observed a nonlinear relationship between the serum 25(OH)D and anemia, with a threshold for 25(OH)D of 50.0 nmol/L existed for anemia. Conclusion: Maternal serum 25(OH)D 〈 50.0 nmol/L may be a risk factor for gestational anemia, and it should be monitored for the high-risk pregnant women.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 3
    In: Food Science & Nutrition, Wiley, Vol. 7, No. 11 ( 2019-11), p. 3759-3765
    Abstract: Interest in the high folate status of pregnant women has increased due to its role in the prevention of neural tube defects (NTDs). The effect of increased red blood cell (RBC) folate status during the second trimester of pregnancy on gestational diabetes mellitus (GDM) remains unclear. We measured RBC folate concentrations by competitive protein‐binding assay and obtained clinical information from electronic medical records. Logistic regression analysis was used to explore the associations of RBC folate concentrations with risks of gestational diabetes mellitus (GDM). We further assessed the potential nonlinear relations between continuous log‐transformed RBC folate concentrations and GDM risk by using the restricted cubic splines. We observed high RBC folate concentrations in GDM patients compared to control group [median (interquartile range, IQR), GDM vs. controls: 1,554.03 (1,240.54–1,949.99) vs. 1,478.83 (1,124.60–1,865.71) nmol/L, p  = .001]. Notably, high folate concentrations were significantly associated with an increased risk of GDM [RR per 1‐ SD increase: 1.16 (1.03, 1.30), p  = .012] after adjustment for maternal age, parity, and body mass index (BMI) at enrollment. In the restricted cubic spline model, a test of the null hypothesis of the linear relationship was rejected ( p  = .001). Our study firstly showed that maternal RBC folate concentrations during the second trimester of pregnancy increase the risk of GDM in a Chinese population. Further randomized clinical trials (RCTs) are warranted to confirm the adverse effect.
    Type of Medium: Online Resource
    ISSN: 2048-7177 , 2048-7177
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2703010-6
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  • 4
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2019
    In:  Scientific Reports Vol. 9, No. 1 ( 2019-03-29)
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2019-03-29)
    Abstract: To date, only three polymorphisms (rs10830962, rs7754840 and rs1470579) are included in the genome-wide association study Catalog ( www.ebi.ac.uk/gwas ). However, the available evidence is limited in pregnant Chinese women. We aimed to explore the associations of three polymorphisms (rs10830962, rs7754840 and rs1470579) with GDM risk in a Chinese population. We conducted a case-control study (964 GDM cases and 1,021 controls) to evaluate the associations of these polymorphisms with GDM risk. A logistic regression model was used to calculate odds ratios (ORs) and their confidence intervals (CIs). After adjustment for age, prepregnancy BMI, parity, abnormal pregnancy history and family history of diabetes, the minor allele of rs10830962 (C  〉  G) demonstrated a significant association with an increased risk of GDM (OR = 1.16, 95% CI = 1.02–1.31, P  = 0.029 in the additive model). However, no significant association was observed between the other two polymorphisms and GDM. Subsequent functional annotation shows that rs10830962 is located in the regulatory elements of pancreatic islets, alters the binding affinity of motifs and regulates SNORA8 expression. Our findings demonstrate that rs10830962 is associated with an increased risk of GDM in the Chinese population. Further functional characterization is warranted to uncover the mechanism of the genotype-phenotype association.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2615211-3
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  • 5
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-04-18)
    Abstract: Whether the maternal vitamin D deficiency is associated with infant birth weight is still an argument. Here, we performed a nested case-control study (545 women who subsequently delivered infant with macrosomia and 1090 controls) to evaluate the association of the maternal serum 25-hydroxyvitamin D [25(OH)D] concentrations with risk of macrosomia. We measured the serum 25(OH)D concentrations by enzyme immunoassays. Logistic regression analysis, receiver-operator characteristic curve analysis and graphical nomogram were used for the statistical analyses. Among women who delivered infant with macrosomia, 71.2% of the women had serum 25(OH)D concentrations 〈 50.0 nmol/L compared with 61.1% of the control women ( P   〈  0.001). For women with concentrations 〈 50.0 nmol/L, they had a 33% increased risk of macrosomia compared with women whose 25(OH)D ranged from 50.0 to 74.9 nmol/L. The risk of macrosomia was significantly increased with the decreasing concentrations of serum 25(OH)D in a dose-dependent manner ( P for trend = 0.001). We also observed a threshold for 25(OH)D of 50.0 nmol/L for delivering infant with macrosomia and a predictive accuracy of the 25(OH)D concentrations included panel, with an area under the ROC curve of 0.712 for delivering infant with macrosomia. In conclusion, maternal serum 25(OH)D 〈 50.0 nmol/L is associated with delivering a macrosomic infant, and vitamin D deficiency should be monitored in pregnant women.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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  • 6
    In: Metabolism, Elsevier BV, Vol. 78 ( 2018-01), p. 95-105
    Type of Medium: Online Resource
    ISSN: 0026-0495
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2049062-8
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  • 7
    Online Resource
    Online Resource
    Mary Ann Liebert Inc ; 2014
    In:  Journal of Interferon & Cytokine Research Vol. 34, No. 5 ( 2014-05), p. 342-348
    In: Journal of Interferon & Cytokine Research, Mary Ann Liebert Inc, Vol. 34, No. 5 ( 2014-05), p. 342-348
    Type of Medium: Online Resource
    ISSN: 1079-9907 , 1557-7465
    Language: English
    Publisher: Mary Ann Liebert Inc
    Publication Date: 2014
    detail.hit.zdb_id: 1483128-4
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  • 8
    In: Journal of Molecular Endocrinology, Bioscientifica, Vol. 62, No. 3 ( 2019-04), p. 137-148
    Abstract: Obesity is a major risk factor for metabolic diseases, while adipocyte differentiation is closely related to obesity occurrence. Long noncoding RNAs (lncRNAs) are a unique class of transcripts in regulation of various biological processes. Using lncRNA microarray, we found lncRNA AC092159.2 was highly expressed in differentiated HPA-v and located ~247 bp upstream of the TMEM18, which was associated with BMI and obesity. We aimed to explore the role of AC092159.2 in adipogenesis and the underlying mechanisms. The effects of AC092159.2 gain- and loss-of-function on HPA-v adipogenesis were determined with lentivirus and siRNA-mediated cell transduction, respectively. Lipid accumulation was evaluated by oil red O staining; the expression of AC092159.2, TMEM18 and several adipogenesis makers in HPA-v were analyzed by qPCR/Western blot. We found that the expression of AC092159.2 gradually increased during HPA-v differentiation, and its expression in omental adipose tissue was positively related with BMI among 48 human subjects. Overexpression of AC092159.2 promoted adipocytes differentiation while knockdown of it led to an adipogenic defect. Moreover, the expression of AC092159.2 and TMEM18 were positively correlated during adipogenic differentiation. AC092159.2 overexpression boosted TMEM18 expression while AC092159.2 knockdown restrained TMEM18 expression. Further rescue experiments showed that TMEM18 knockdown partially restrained adipogenic differentiation in AC092159.2 overexpressed HPA-v and adipogenic defect caused by AC092159.2 knockdown could be rescued by TMEM18 overexpression. Luciferase reporter assays revealed that AC092159.2 had a transcriptional activation effect on TMEM18. We concluded that lncRNA AC092159.2 promoted human adipocytes differentiation possibly by regulating TMEM18.
    Type of Medium: Online Resource
    ISSN: 0952-5041 , 1479-6813
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2019
    detail.hit.zdb_id: 1478171-2
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  • 9
    In: Journal of Cellular Physiology, Wiley, Vol. 233, No. 12 ( 2018-12), p. 9383-9389
    Abstract: Folate supplementation is recommended before and during early pregnancy to prevent neural tube defects, but the effect of red blood cell (RBC) folate on large for gestational age (LGA) is still unknown. We performed a nested case‐control study including 542 LGA cases and 1,084 appropriate for gestational age (AGA) controls to examine the association of RBC folate concentrations with risk of LGA. Then, male offspring of dams fed basic folic acid (2 mg/kg, control) or 10‐fold folic acid (20 mg/kg, HFol) diet before and during pregnancy were used to explore the effect of high folate intake on birth weight and long‐term effects. We observed higher RBC folate concentrations in the cases compared to controls ( p  = 0.039). After adjustment for maternal age, BMI at enrollment, gestational weeks at enrollment, gestational weeks at delivery and infant gender, higher RBC folate levels were significantly associated with increased risk of LGA ( P trend   = 0.003). Interestingly, male offspring of HFol dams showed the higher birth weight, elevated levels of post loading blood glucose at 9 and 13 weeks post‐weaning and increased triglyceride (TG) and total cholesterol (TC) levels at 17 weeks post‐weaning. Furthermore, we observed that high folate intake increased the proliferation and differentiation of adipose cells. Our results suggest that maternal high folate intake confers the risk of LGA birth and accelerates the development of obesity in male offspring.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 10
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-01-10)
    Abstract: To evaluate the effects of maternal vitamin D deficiency on body fat and adipogenesis in offspring rats, and explore the potential mechanism, we constructed a vitamin D deficient rat model and performed metabolic activity evaluation, body fat monitoring, biochemical analysis, adipogenesis assay, methylation microarray and RNA-seq for their offspring rats. We found the weight of vitamin D deficient (VDD) offspring was gradually higher than that of control (CLT) offspring, and the difference was significant since 10 weeks old. When compared with CTL offspring, the 24 h heat production, peak blood glucose, adipose tissue volume and blood lipid indexes were significantly increased in VDD offspring at 14 weeks old. Moreover, a significant increase in proliferation rate and number of lipid droplets for pre-adipocytes was also observed in VDD offspring group. DNA methylation profiling showed that compared to CTL group, 608 promoters and 204 CpG islands were differentially methylated in the VDD group, involving 305 genes. When combined with the results of RNA-seq, 141 genes of the methylated genes were differentially expressed. In conclusion, vitamin D deficiency during pregnancy may promote the proliferation and differentiation of pre-adipocytes, which may be associated with methylation alterations of genes, ultimately leading to offspring obesity.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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