Area under curve (AUC) and 95% confidence interval (CI) for Indian Fatty Liver Index (IFLI), Fatty Liver Index (FLI), Lipid Accumulation Product (LAP), Liver Fat (LF) (%) and NAFLD Fat Score (NFS).

<p>A, IFLI-clinical; B, FLI; C, IFLI- clinical and biochemical; D, LAP; E, % LF and F, NFS.</p

Body composition between cases (n = 162) and controls (n = 173) was estimated by using whole body dual-energy X-ray absorptiometry scan.

<p>Body composition between cases (n = 162) and controls (n = 173) was estimated by using whole body dual-energy X-ray absorptiometry scan.</p

Adjusted odds ratios (ORs) and 95% confidence intervals (CI) calculated using multivariate logistic regression analyses.

<p>Adjusted ORs were adjusted taking in consideration HOMA, hs CRP, diastolic blood pressure, weight, BMI, hip circumference, mid thigh circumference and total cholesterol.</p><p>Adjusted odds ratios (ORs) and 95% confidence intervals (CI) calculated using multivariate logistic regression analyses.</p

Comparison of skinfold thickness between cases (n = 162) and controls (n = 173).

<p>Central (sum of subscapular and suprailiac) and peripheral skinfold thicknesses (sum of biceps and triceps) were calculated.</p

Comparison of Indian Fatty Liver Index, Fatty Liver Index, Lipid Accumulation Index, Liver Fat (%) and NAFLD Liver Fat Score prediction scores.

<p>All p values are <0.001. CB, Clinical and biochemical; AUC, area under curve; LR, likelihood ratio (+, positive; -; negative).</p><p>¹n, 216 with and 280 without suspected liver disease; fatty liver was diagnosed by ultrasonography (17).</p><p>²n, 588; definition of fatty liver was based on liver ultrasonography (18).</p><p>³n, 359 non-diabetic, 111 type 2 diabetes; liver fat content was measured using proton magnetic resonance spectroscopy (19).</p><p>Comparison of Indian Fatty Liver Index, Fatty Liver Index, Lipid Accumulation Index, Liver Fat (%) and NAFLD Liver Fat Score prediction scores.</p

Biochemical profile.

<p>All values except that mentioned in line 2 are from fasting plasma levels. Values are given as the mean ±standard deviation.</p><p>* Wilcoxon rank-sum (Mann-Whitney) test, Median (minimum- maximum). P value <0.05 is statistically significant. LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; VLDL, very-low density lipoprotein; ALT, alanine transaminase; AST, aspartate transaminase; GGT, γ glutamyl transpeptidase; HOMA-IR, homoeostasis modal assessment for insulin resistance; Hs-CRP, high sensitive C- reactive protein.</p><p>┼Blood taken 2 hours after first bite of standard breakfast.</p><p>Biochemical profile.</p

Demographic, clinical and anthropometric profiles.

<p>*All values are given as the number (%). P value <0.05 is statistically significant. Values are given as the mean ±standard deviation. MTC, mid thigh circumference; MAC, mid arm circumference</p><p>Demographic, clinical and anthropometric profiles.</p

Odds Ratios for obesity, abdominal obesity, subcutaneous adiposity and LBM according to <i>Myostatin</i> (A55T & K153R) genotypes.

<p> SCT Obesity, subcutaneous obesity; LBM, lean body mass.</p

Interactions between the FTO and GNB3 Genes Contribute to Varied Clinical Phenotypes in Hypertension

<div><p>Background</p><p>The genes <i>FTO</i> and <i>GNB3</i> are implicated in essential hypertension but their interaction remains to be explored. This study investigates the role of interaction between the two genes in the pathophysiology of essential hypertension.</p><p>Methods/Principal Findings</p><p>In a case-control study comprising 750 controls and 550 patients, interaction between the polymorphisms of <i>FTO</i> and <i>GNB3</i> was examined using multifactor dimensionality reduction (MDR). The influence of interaction on clinical phenotypes like systolic and diastolic blood pressure, mean arterial pressure and body mass index was also investigated. The 3-locus MDR model comprising <i>FTO</i> rs8050136C/A and <i>GNB3</i> rs1129649T/C and rs5443C/T emerged as the best disease conferring model. Moreover, the interacted-genotypes having either 1, 2, 3, 4 or 5 risk alleles correlated with linearly increasing odds ratios of 1.91 (<i>P</i> = 0.027); 3.93 (<i>P</i> = 2.08E–06); 4.51 (<i>P</i> = 7.63E–07); 7.44 (<i>P</i> = 3.66E–08) and 11.57 (<i>P</i> = 1.18E–05), respectively, when compared with interacted-genotypes devoid of risk alleles. Furthermore, interactions among haplotypes of <i>FTO</i> (H₁−₉) and <i>GNB3</i> (H_a-d) differed by >1.5-fold for protective-haplotypes, CTGGC+TC [H₂+H_a] and CTGAC+TC [H₄+H_a] (OR = 0.39, <i>P</i> = 0.003; OR = 0.22, <i>P</i> = 6.86E–05, respectively) and risk-haplotypes, AAAGC+CT [H₃+H_c] and AAAGC+TT [H₃+H_d] (OR = 2.91, <i>P</i> = 9.98E–06; OR = 2.50, <i>P</i> = 0.004, respectively) compared to individual haplotypes. Moreover, the effectiveness of gene-gene interaction was further corroborated with a 1.29-, 1.25- and 1.38-fold higher SBP, MAP and BMI, respectively, in patients having risk interacted-haplotype H₃+H_c and 2.48-fold higher SBP having risk interacted-haplotype H₃+H_d compared to individual haplotypes.</p><p>Conclusion</p><p>Interactions between genetic variants of <i>FTO</i> and <i>GNB3</i> influence clinical parameters to augment hypertension.</p></div

Flow diagram explaining the subject recruitment, selection and reasons for exclusion.

<p>Flow diagram explaining the subject recruitment, selection and reasons for exclusion.</p