[Early nutrition: the role of genetics and epigenetics].
Many adult diseases seem to be associated with early nutrition and the subsequent growth pattern. Epidemiological studies hypotized that babies with intrauterine and/or neonatal growth retardation may be at greater risk of metabolic syndrome later in life. According to the Barker's "thrifty phenotype hypotesis" early malnutrition, whereas inducing physiological compensation by the promotion of early survival, appears to confer greater susceptibility to adults diseases. Epigenetics, that is the interindividual variation in DNA methylation patterns and chromatin remodelling, provide a potential explanation for how environmental factors can modify the risk for development of many common diseases. Beginning from animal models, many studies concerning early nutrition, epigenetic modifications and genes expression have been carried out. Maternal undernutrition during pregnancy, especially in the peri-implantation period, not only causes a prolonged growth retardation but also modifies the programming of biochemical mechanisms related to endocrine-metabolic control. Human studies have demonstrated the role played by IGF-1 as indicator of nutritional status and fetal/postnatal growth retardation. It has been reported that alterations in IGF axis, which predispose to adults diseases, may be due to an alterated epigenetic regulation that can modify IGF expression. Despite the critical inter-relation between early nutrition, growth, development, and subsequent health, there are few data on the influence of early nutrition on the modifications of the epigenetic gear. Furthermore it is hoped for a bigger attention to the early nutrition to prevent the development of diseases later in life.
Liotto
N
N
Institute of Pediatrics and Neonatology, Fondazione IRCCS "Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena," University of Milan, Italy.
Miozzo
M
M
Giannì
M L
ML
Taroni
F
F
Morlacchi
L
L
Piemontese
P
P
Roggero
P
P
Mosca
F
F
D000328:Adult; D000818:Animals; D044127:Epigenesis, Genetic; D019317:Evidence-Based Medicine; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000517:prevention & control; D018507:Gene Expression Regulation, Developmental; D005819:Genetic Markers / Q000235:genetics; D006801:Humans; D007227:Infant Nutritional Physiological Phenomena / Q000235:genetics; D007231:Infant, Newborn; D007334:Insulin-Like Growth Factor I / Q000235:genetics*; D007335:Insulin-Like Growth Factor II / Q000235:genetics*; D044342:Malnutrition / Q000235:genetics / Q000517:prevention & control; D024821:Metabolic Syndrome / Q000235:genetics / Q000517:prevention & control; D010641:Phenotype; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000235:genetics*; D012307:Risk Factors; D014158:Transcription, Genetic
D005819:Genetic Markers; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II