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Table 2 Summary of effects of selected dietary factors on DNA methylation and histone modifications in animals and in vitro systems

From: Epigenetics and inheritance of phenotype variation in livestock

Nutrient/diet component Observation relevant to DNA methylation Refs.
Methyl donor Maternal supplementation with methyl donors reversed the effects of maternal bisphenol-A exposure during pregnancy on methylation at the Avy of the offspring [193]
Folic acid Changes in tp53 gene expression and DNA methylation status of intrauterine growth retarded rats were reversed by dietary folic acid supplementation [194]
  Folate deficiency did not alter genomic DNA methylation in the liver of BALB/c mice [195]
Selenium Se inhibits DNMT1 activity in vitro from rat liver and Friend erythroleukaemic cells and in prostate cancer cells causes induction of GSTP1, APC and CSR1 gene promoter demethylation and reduction in histone deacetylases (HDAC) activity leading to increased acetylation of H3K9 and gene expression [196]
Protein Dietary supplementation with folic acid prevented hypermethylation in imprinting control region of IGF2 and H19 genes with low-protein diet only [197]
  Promoters of 204 genes were differentially methylated in murine foetal liver in response to low-protein feeding during pregnancy. The promoter of the liver X-receptor alpha was significantly hypermethylated by the protein restriction [198]
Fatty acids Fat exposure during development induces persistent changes in hepatic polyunsaturated fatty acid status in offspring through epigenetic regulation of fatty acid desaturase gene (Fads2) transcription [122]
  Observation relevant to histone modifications Refs.
  Model of porcine kidney fibroblasts (PKFs)
NaBu-induced hyperacetylation up-regulates Wilms' tumor 1 (WT1) gene expression essential for the development of kidney fibroblasts (PKFs) suggesting histone acetylation mediation in the transcriptional modulation of WT1 in porcine kidney cells  
  Model of mouse adipose tissue
Mice heterozygous for a mutation in Trim28 (known as KAP1 or TIF1-β), an epigenetic-modifier complex that directs a repressive chromatin state, develop liver steatosis, adipocyte hypertrophy and impaired glucose tolerance