7 research outputs found

    Clinical features of the study population according to ethnicity and <i>PNPLA3</i> rs738409 genotype.

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    *<p>β€Š=β€Šlog transformed and adjusted for age, gender, BMI, glucose tolerance. **β€Š=β€ŠSquare root transformed and adjusted for age, gender, BMI, glucose tolerance. GT β€Š=β€Š glucose tolerance. NGTβ€Š=β€Š normal glucose tolerance, IGTβ€Š=β€Š impaired glucose tolerance, T2D β€Š=β€Š type 2 diabetes.</p

    Interaction between <i>PNPLA3</i> rs738409 and n-6/n-3 PUFA in modulating ALT levels.

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    <p>The figure shows a different degree of regression between ALT (log10) and n-6/n-3 PUFA (log10) in the three genotypes. In the CC (Panel A) and CG (Panel B) group there was no association between ALT and n-6/n-3 PUFA (r2β€Š=β€Š0.0006, pβ€Š=β€Š0.91 and r2β€Š=β€Š0.015, pβ€Š=β€Š0.21 respectively). Only in the GG group (Panel C) there was a strong association between HFF% and n-6/n-3 PUFA (r2β€Š=β€Š 0.40, pβ€Š=β€Š0.006).</p

    Interaction between <i>PNPLA3</i> rs738409 and n-6/n-3 PUFA in modulating HFF%.

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    <p>The figure shows a different degree of regression between HFF% (square root) and n-6/n-3 PUFA (log10) in the three genotypes. In the CC (Panel A) and CG (Panel B) group there was no association between HFF% and n-6/n-3 PUFA (r2β€Š=β€Š0.0004, pβ€Š=β€Š0.86 and r2β€Š=β€Š0.018, pβ€Š=β€Š0.39, respectively). Only in the GG group (Panel C) there was a strong association between HFF% and n-6/n-3 PUFA (r2β€Š=β€Š 0.45, pβ€Š=β€Š0.001).</p

    Clinical and laboratory characteristics of obese patients subdivided by PNPLA3 I148M genotype.

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    <p>Values are expressed as means Β± standard deviations. GLM analysis including gender, age and pubertal stage as covariates has been used to compare continuous variables. Abbreviations: BMI-SDS: Body Mass Index Standard Deviation Scores; W/Hr: Waist circumference to height ratio; HOMA: homeostatic model of assessment of insulin resistance index; WBISI: whole body insulin sensitivity index; HDL-C: high density lipoprotein-cholesterol; ALT: alanine transaminase; AST: aspartate transaminase; Gamma-GT: Gamma-Glutamyl transferase.</p><p>*WBISI was available in 497 patients.</p

    Risk of pathologic ALT levels in 1048 obese children stratified in six categories according to fat abdominal size (W/Hr) and PNPLA3 genotype.

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    <p>ALT (alanine transaminase) values are expressed as means Β± standard deviations. Logistic regression analysis has been used to calculate the Odds Ratios (OR) to have ALT>40 UI/L for each category of patients (from I to VI), compared to the entire cohort of children.</p

    Clinical and laboratory characteristics of the 1048 children involved in the study.

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    <p>Values are expressed as means Β± standard deviations. Ranges are in brackets. Abbreviations: BMI-SDS: Body Mass Index Standard Deviation Scores; W/Hr: Waist circumference to height ratio; HOMA-IR: homeostatic model of assessment of insulin resistance index; WBISI: whole body insulin sensitivity index; HDL-C: high density lipoprotein-cholesterol; ALT: alanine transaminase; AST: aspartate transaminase; Gamma-GT: Gamma-Glutamyl transferase. * WBISI was available in 497 patients.</p

    Association between ALT levels and W/Hr, HOMA and BMI-SDS according to the PNPLA3 genotype.

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    <p><b>A</b>: Regression analysis describing the relationship between ALT levels and W/Hr in patients homozygous for <i>PNPLA3</i> M variant, heterozygous, and homozygous for PNPLA3 I variant. The regression between ALT levels and W/Hr in the group of patients homozygous for <i>PNPLA3</i> M/M is described by the equation yβ€Š=β€Š4.6+2.4*Γ— (rβ€Š=β€Š0.36; pβ€Š=β€Š0.00001). The equation for <i>PNPLA3</i> I/M was yβ€Š=β€Š3.7+1.4*Γ— (rβ€Š=β€Š0.22; pβ€Š=β€Š0.00001). The equation for PNPLA3 I/I was yβ€Š=β€Š3.4+1.1*Γ— (rβ€Š=β€Š0.17; pβ€Š=β€Š0.0005). The comparison between the three regression lines is significant (pβ€Š=β€Š0.0045). <b>B</b>: Regression analysis describing the relationship between ALT levels and HOMA-IR in patients homozygous for <i>PNPLA3</i> M variant, heterozygous, and homozygous for PNPLA3 I variant. The regression between ALT levels and HOMA-IR in the group of patients homozygous for <i>PNPLA3</i> M/M is described by the equation yβ€Š=β€Š3.2+0.14*Γ— (rβ€Š=β€Š0.18; pβ€Š=β€Š0.02). The equation for <i>PNPLA3</i> I/M was yβ€Š=β€Š3.0+1.12*Γ— (rβ€Š=β€Š0.16; pβ€Š=β€Š0.001). The equation for PNPLA3 I/I was yβ€Š=β€Š2.9+0.16*Γ— (rβ€Š=β€Š0.23; pβ€Š=β€Š0.00005). The three equations are not significantly different as to slopes (pβ€Š=β€Š0.7). <b>C</b>: Regression analysis describing the relationship between ALT levels and BMI z-score in patients homozygous for <i>PNPLA3</i> M variant, heterozygous, and homozygous for PNPLA3 I variant. The regression between ALT levels and BMI z-score in the group of patients homozygous for <i>PNPLA3</i> M/M is described by the equation yβ€Š=β€Š3.1+0.24*Γ— (rβ€Š=β€Š0.01; pβ€Š=β€Š0.13). The equation for <i>PNPLA3</i> I/M was yβ€Š=β€Š3.1+0.17*Γ— (rβ€Š=β€Š0.08; pβ€Š=β€Š0.14). The equation for PNPLA3 I/I was yβ€Š=β€Š2.9+0.17*Γ— (rβ€Š=β€Š0.09; pβ€Š=β€Š0.04). The three equations are not significantly different as to slopes (pβ€Š=β€Š0.5).</p
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