131 research outputs found

    Distribution of the genetic predisposition score (GPS) and the cumulative effects of risk alleles from the nine variants on BMI z-scores and Waist circumference z-scores.

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    <p>The genetic predisposition score (GPS, n: 1 634 adolescents) was constructed by summing the effect alleles of each SNP ( = BMI-increasing alleles defined in the original genome-wide association studies). (rs4074134 near <i>BDNF</i>, rs17782313 near <i>MC4R</i>, rs987237 near <i>TFAP2B</i>, rs1121980 in <i>FTO</i>, rs2815752 near <i>NEGR1</i>, rs6548238 near <i>TMEM18</i>, rs10838738 in <i>MTCH2</i>, rs10938397 near <i>GNPDA2</i>, rs11084753 near <i>KCTD15</i>).</p

    Associations of the individual obesity-susceptibility SNPs and the GPS<sup>1</sup> with adiposity-related traits<sup>2</sup> in adolescence of Young-HUNT1<sup>3</sup>.

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    1<p>The genetic predisposition score (GPS) is the sum of effect alleles from each of the nine individual SNPs.</p>2<p>Age and sex specific z-scores of BMI and waist circumference in adolescence.</p>3<p>Number of participants: for individual SNPs = 1643 and for GPS = 1634 (those missing more than 3 SNPs excluded).</p><p>The linear regression models were adjusted for pubertal maturity regarding BMI and additionally also for height regarding WC, assuming an additive effect. Pregnant participants were excluded.</p><p>Chrom: chromosome.</p><p>Comparable effect sizes in the literature:</p>a<p>den Hoed et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046912#pone.0046912-den1" target="_blank">[21]</a>;</p>b<p>Zhao et al.</p>c<p>Willer et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046912#pone.0046912-Willer1" target="_blank">[17]</a>.</p

    Genotype information and quality control statistics for the 9 obesity-susceptibility variants included in the study.

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    <p>Article reference: 1) Loos et al., 2009; 2) Hinney et al., 2007; 3) Loos et al., 2008; 4) Willer et al., 2009; 5) Zhao et al., 2009; 6) Thorleifson et al., 2009;</p><p>HWE: Hardy-Weinberg equilibrium; Call-rate: rate of successful genotyping. All variants passed initial quality-control criteria with a call-rate ≥95% and genotype distribution were in Hardy-Weinberg equilibrium (P>0.05). The genotype distribution and effect allele frequencies varied from 17.7% for rs987237 to 83.7% for rs654238), which were in consistency with previous reports.</p

    Associations of the individual obesity-susceptibility SNPs and the GPS<sup>1</sup> with adiposity-related traits<sup>2</sup> in young adulthood (HUNT3)<sup>3</sup>.

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    1<p>The genetic predisposition score (GPS) is the sum of effect alleles from each of the nine individual SNPs.</p>2<p>Sex specific z-scores of BMI and waist circumference in young adulthood.</p>3<p>Number of participants: for individual SNPs = 1643 and for GPS = 1634 (those missing more than 3 SNPs excluded).</p><p>The linear regression models were adjusted for age regarding BMI and additionally also for height regarding WC, assuming an additive effect.</p><p>Pregnant participants were excluded.</p><p>Chrom: chromosome.</p><p>Comparable effect sizes in the literature:</p>d<p>Li et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046912#pone.0046912-Li2" target="_blank">[35]</a>;</p>e<p>Lindgren et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046912#pone.0046912-Lindgren1" target="_blank">[19]</a>.</p

    Associations of the individual obesity susceptibility SNPs and the GPS<sup>1</sup> with change in adiposity-related traits<sup>2</sup> from adolescence into adulthood<sup>3</sup>.

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    1<p>The genetic predisposition score (GPS) is the sum of effect alleles from each of the nine individual SNPs.</p>2<p>Delta BMI and delta WC are differences between sex-specific z-scores in young adulthood and age-and-sex-specific z-scores in adolescence of BMI and WC respectively.</p>3<p>Number of participants: for individual SNPs = 1643 and for GPS = 1634 (those missing more than 3 SNPs excluded).</p><p>The linear regression models were adjusted for pubertal development and age-difference between adolescence and adulthood regarding change BMI and additionally also for height regarding change WC, assuming an additive effect. Pregnant participants were excluded.</p><p>Chrom: chromosome.</p

    Descriptive statistics of participants stratified by zygosity and gender.

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    <p>Data are means and standard deviation (SD).</p><p>*Within-pair analysis of same sex pairs (men n = 156, women n = 170), (DZ n = 91, MZ n = 235) MZ: Monozygotic twins; DZ: dizygotic twins.</p

    Associations (β –coefficients; 95% CI) between within-twin pair difference in birth weight (kg) and the within-twin pair difference in adult hand grip strength or fat free mass stratified by sex and zygosity.

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    <p>Model 1 – unadjusted.</p><p>Model 2 – adjusted for within twin pair difference in adult height.</p><p>Model 3 – adjusted for within twin pair difference in adult fat-free mass.</p><p>Linear regression β coefficients represents the difference in adult grip strength (kg) or fat free mass (kg) per 1 kg difference in birth weight between twin 1 and twin 2 with 95% Confidence Intervals (MZ Monozygotic twins; DZ: dizygotic twins).</p

    Case-control analyses of <i>PCSK1</i> rs6234 with obesity and overweight.

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    <p>The ORs are odds ratios that represent the effects of risk allele (G-allele) based on an additive model, in which individuals homozygous for CC were coded as 0, heterozygous individuals CG were coded as 1, and individuals homozygous for GG were coded as 2; The ORs and <i>P</i> values were adjusted for age, region and sex (where appropriate).</p><p>MAF, minor allele frequency.</p
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