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Epigenetic modifications alter transcriptional activity and contribute to the effects of environment on the individual risk of obesity and Type 2 Diabetes (T2D). Here, we have estimated the  in vivo  effect of a fat-enriched diet (HFD) on the expression and the epigenetic regulation of the  Ankyrin repeat domain 26 (Ankrd26 ) gene, which is associated with the onset of these disorders. In visceral adipose tissue (VAT), HFD exposure determined a specific hyper-methylation of  Ankrd26  promoter at the −436 and −431 bp CpG sites (CpGs) and impaired its expression. Methylation of these 2 CpGs impaired binding of the histone acetyltransferase/transcriptional coactivator p300 to this same region, causing hypo-acetylation of histone H4 at the  Ankrd26  promoter and loss of binding of RNA Pol II at the  Ankrd26  Transcription Start Site (TSS). In addition, HFD increased binding of DNA methyl-transferases (DNMTs) 3a and 3b and methyl-CpG-binding domain protein 2 (MBD2) to the  Ankrd26  promoter. More importantly,  Ankrd26  down-regulation enhanced secretion of pro-inflammatory mediators by 3T3-L1 adipocytes as well as in human sera. Thus, in mice, the exposure to HFD induces epigenetic silencing of the  Ankrd26  gene, which contributes to the adipose tissue inflammatory secretion profile induced by high-fat regimens.

Specific CpG hyper-methylation leads to Ankrd26 gene down-regulation in white adipose tissue of a mouse model of diet-induced obesity