51 research outputs found

    Summary of estimates from the different types of analysis.

    No full text
    <p>Lines represent 95% CIs. CI, confidence interval; MR, Mendelian randomization; OR, odds ratio; SNP, single nucleotide polymorphism.</p

    Sensitivity analysis.

    No full text
    <p>Upper panels show scatter plots of genetic association with type 1 diabetes over genetic associations with SDS-BMI. Lines represent 95% confidence intervals. The lower panels show funnel plots of instrumental variable precision against instrumental variable estimates for genetic associations between SDS-BMI and type 1 diabetes. In all panels, the dashed line represents slopes/estimates for inverse-variance-weighted analysis, and the dotted line represents the slope from MR Egger regression. rs13130484 and rs13107325 were nominally associated (<i>p</i> < 0.01) with education and marked with blue color. IV, instrumental variable; SDS-BMI, age- and sex-specific standard deviation score of childhood body mass index; SNP, single nucleotide polymorphism; T1D, type 1 diabetes.</p

    Association of childhood adiposity-related genetic variants with “ever smoker.”

    No full text
    <p>Lines represent 95% confidence intervals. Note that because of the large number of SNPs investigated, the threshold for nominal significance was set to <i>p</i> < 0.01. No SNP was alone associated with smoking, but the combined score showed a positive association. BMI, body mass index; CI, confidence interval; OR, odds ratio; SNP, single nucleotide polymorphism.</p

    Overview of the metabolites being associated with at least one of the five MetS criteria.

    No full text
    The criteria are given together with sum of criteria. The table was sorted on sum of criteria. (DOCX)</p

    Relationships between the 15 validated metabolites being related to all five components in the metabolic syndrome (MetS) and incident atherosclerotic cardiovascular disease in the EpiHealth cohort.

    No full text
    Relationships between the 15 validated metabolites being related to all five components in the metabolic syndrome (MetS) and incident atherosclerotic cardiovascular disease in the EpiHealth cohort.</p

    Role of peroxisome proliferator-activated receptor gamma Pro12Ala polymorphism in human adipose tissue: assessment of adipogenesis and adipocyte glucose and lipid turnover

    No full text
    <p>The protective mechanisms of peroxisome proliferator-activated receptor gamma (PPARγ) Pro12Ala polymorphism in type 2 diabetes (T2D) are unclear. We obtained subcutaneous adipose tissue (AT) before and 3 h after oral glucose (OGTT) in carriers and non-carriers of the Ala allele (12 Pro/Pro, 15 Pro/Ala, and 13 Ala/Ala). Adipogenesis, adipocyte glucose uptake and lipolysis as well as PPARγ target gene expression were investigated and compared between the genotype groups. During fasting and post-OGTT, neither basal nor insulin-stimulated adipocyte glucose uptake differed between genotypes. Compared to fasting, a decreased hormone-sensitive lipase gene expression in Pro/Pro (p < 0.05) was accompanied with a higher antilipolytic effect of insulin post-OGTT (p < 0.01). The adipocyte size was similar across groups. Preadipocyte differentiation rates between Pro/Pro and Ala/Ala were unchanged. In conclusion, no major differences in AT differentiation, glucose uptake, lipolysis or expression of PPARγ target genes were observed between different PPARγ Pro12Ala genotypes. Albeit small, our study may suggest that other pathways in AT or effects exerted in other tissues might contribute to the Pro12Ala-mediated protection against T2D.</p
    corecore