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Fig. 4 | Clinical Epigenetics

Fig. 4

From: Epigenetic silencing of the ANKRD26 gene correlates to the pro-inflammatory profile and increased cardio-metabolic risk factors in human obesity

Fig. 4

ANKRD26 gene expression, promoter methylation, and cardio-metabolic risk. a Relationship between ANKRD26 expression and TG/HDL-C ratio was assessed in lean (n = 14) and obese individuals (n = 20) by covariate-adjusted Spearman’s rank-order correlation adjusted for age (n = 34; r = − 0.728; p < 0.001). b Relationships between TG/HDL-C ratio and the combined DNA methylation at the CpGs − 689, − 659, and − 651 in lean (n = 14) and obese individuals (n = 20) was assessed by covariate-adjusted Spearman’s rank-order correlation adjusted for age. r = 0.666, p < 0.001. c ANKRD26 mRNA levels in 11 individuals with the TG/HDL-C > 3.0 and in 23 individuals with the TG/HDL-C < 3.0. Values are expressed in absolute units (AU) and their distribution within each group is represented by box plots. Box plots show median (line within the box), quartiles (upper and lower box boundaries), and extreme values (whiskers). Statistical differences between the two groups were tested using nonparametric quantile regression, with inference based on median, to adjust for BMI. p = 0.016 vs. individuals with the TG/HDL-C < 3.0. d Bisulfite sequencing methylation analysis of the ANKRD26 CpG sites, − 689, − 659, and − 651 bp from the TSS in converted genomic DNA from PBL of 11 individuals with TG/HDL-C > 3.0 and in 23 individuals with the TG/HDL-C < 3.0. Results are means ± SD. Statistical difference between the means of the two groups was assessed by classical OLS regression model to adjust for BMI. *p < 0.05 and ***p < 0.001 vs. individuals with TG/HDL-C < 3.0

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