Early nutrition and epigenetic programming: chasing shadows.
OBJECTIVE
The ways in which epigenetic modifications fix the effects of early environmental events, ensuring sustained responses to transient stimuli, which result into modified gene expression patterns and phenotypes later in life, is a topic of considerable interest. This review focuses on recently discovered mechanisms and calls into question prevailing views about the dynamics, positions and functions of relevant epigenetic marks.


RESULTS
Animal models, including mice, rats, sheep, pigs and rabbits, remain a vital tool for studying the influence of early nutritional events on adult health and disease. Most epigenetic studies have addressed the long-term effects on a small number of epigenetic marks, at the global or individual gene level, of environmental stressors in humans and animal models. They have demonstrated the existence of a self-propagating epigenetic cycle. In parallel, an increasing number of studies based on high-throughput technologies and focusing on humans and mice have revealed additional complexity in epigenetic processes, by highlighting the importance of crosstalk between the different epigenetic marks. In recent months, a number of studies focusing on the developmental origin of health and disease and metabolic programming have identified links between early nutrition, epigenetic processes and long-term illness.


CONCLUSIONS
Despite recent progress, we are still far from understanding how, when and where environmental stressors disturb key epigenetic mechanisms. Thus, identifying the original key marks and their changes throughout development, during an individual's lifetime or over several generations, remains a challenging issue.
Attig
Linda
L
BDR Biologie du Développement et Reproduction, Developmental Biology and Reproduction, UMR INRA-ENVA-CNRS 1198, Domaine de Vilvert, Jouy en Josas, France.
Gabory
Anne
A
Junien
Claudine
C
D000328:Adult; D000818:Animals; D019175:DNA Methylation; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000235:genetics*; D015870:Gene Expression; D018507:Gene Expression Regulation, Developmental; D020022:Genetic Predisposition to Disease; D006657:Histones; D006801:Humans; D007223:Infant; D007227:Infant Nutritional Physiological Phenomena / Q000235:genetics*; D010641:Phenotype; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000235:genetics*
D006657:Histones