title: Nutrition, epigenetics, and metabolic syndrome.
abstract: CONCLUSIONS
  Epidemiological and animal studies have demonstrated a close link between maternal nutrition and chronic metabolic disease in children and adults. Compelling experimental results also indicate that adverse effects of intrauterine growth restriction on offspring can be carried forward to subsequent generations through covalent modifications of DNA and core histones.
  
  
  BACKGROUND
  DNA methylation is catalyzed by S-adenosylmethionine-dependent DNA methyltransferases. Methylation, demethylation, acetylation, and deacetylation of histone proteins are performed by histone methyltransferase, histone demethylase, histone acetyltransferase, and histone deacetyltransferase, respectively. Histone activities are also influenced by phosphorylation, ubiquitination, ADP-ribosylation, sumoylation, and glycosylation. Metabolism of amino acids (glycine, histidine, methionine, and serine) and vitamins (B6, B12, and folate) plays a key role in provision of methyl donors for DNA and protein methylation.
  
  
  RESULTS
  Disruption of epigenetic mechanisms can result in oxidative stress, obesity, insulin resistance, diabetes, and vascular dysfunction in animals and humans. Despite a recognized role for epigenetics in fetal programming of metabolic syndrome, research on therapies is still in its infancy. Possible interventions include: 1) inhibition of DNA methylation, histone deacetylation, and microRNA expression; 2) targeting epigenetically disturbed metabolic pathways; and 3) dietary supplementation with functional amino acids, vitamins, and phytochemicals.
  
  
  CONCLUSIONS
  Much work is needed with animal models to understand the basic mechanisms responsible for the roles of specific nutrients in fetal and neonatal programming. Such new knowledge is crucial to design effective therapeutic strategies for preventing and treating metabolic abnormalities in offspring born to mothers with a previous experience of malnutrition.
authors: State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing, China.
authors: Junjun
authors: J
authors: Wang
authors: Zhenlong
authors: Z
authors: Wu
authors: Defa
authors: D
authors: Li
authors: Ning
authors: N
authors: Li
authors: Scott V
authors: SV
authors: Dindot
authors: M Carey
authors: MC
authors: Satterfield
authors: Fuller W
authors: FW
authors: Bazer
authors: Guoyao
authors: G
authors: Wu
mesh_terms: D000818:Animals; D044127:Epigenesis, Genetic / Q000235:genetics; D005260:Female; D006801:Humans; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000209:etiology* / Q000235:genetics* / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics / Q000378:metabolism