Epigenetics regulates imprinting which modulates embryonic development and cell specific functions as well as gene expression across life; specific cell functions due to differentiation are maintained by “epigenetic memory” and inherited during replication. This mechanism depends on the availability of functional groups that can be obtained from food oxidation. The exposome, consisting in the exposure to factors like food, environment and stress etc., significantly modulates our epigenome, and in specific period of life ( i.e. neonatal period, pregnancy), these epigenetic changes can impact health at adult age and they might be inherited by progenies. A link between early life epigenetics and the development of obesity and cardiovascular diseases later in life has been observed in offspring born from malnourished mothers (1). Similarly, stress and xenobiotic exposure during neonatal age can modify neuronal development in sensitive subjects (2,3). Nutri-epigenomics studies the impact of micro- and macro-nutrients on gene expression; functional groups (i.e. methyl, acetyl, phosphate, etc) deriving from food oxidation can link with aminoacidic residues at histone tails modify chromatin structure. Furthermore, cytosine methylation at CpG island can modulate gene expression and inhibits transposon mobility, resulting in a proper functionality and genome stability. Studies on experimental models highlight that high fat or low protein diet can lead to disease development in exposed parents and in their offspring due to epigenetic changes; disease can be controlled inhibiting epigenetic inheritance linked to the observed disorder (4). Epigenetic biomarkers (i.e. RXRA) at umbilical cord tissue have been identified and correlated to the increased susceptibility to obesity in adolescents and other diseases at adult age (5). Referenze 1. Tobi EW et al., Human Molecular Genetics, 2009;18 (21): 4046-4053 2. Bordoni L, Gabbianelli R. Biochimie 2019; 160:156-171. 3. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 4. Guida MC et al., Nature Communications (2019)10:193 | https://doi.org/10.1038/s41467-018-08128-3. 5. Godfrey KM, et al. Diabetes. 2011;60(5):1528–1534. doi:10.2337/db10-0979.
Nutri-epigenomics: can we program health?
Gabbianelli R
2019-01-01
Abstract
Epigenetics regulates imprinting which modulates embryonic development and cell specific functions as well as gene expression across life; specific cell functions due to differentiation are maintained by “epigenetic memory” and inherited during replication. This mechanism depends on the availability of functional groups that can be obtained from food oxidation. The exposome, consisting in the exposure to factors like food, environment and stress etc., significantly modulates our epigenome, and in specific period of life ( i.e. neonatal period, pregnancy), these epigenetic changes can impact health at adult age and they might be inherited by progenies. A link between early life epigenetics and the development of obesity and cardiovascular diseases later in life has been observed in offspring born from malnourished mothers (1). Similarly, stress and xenobiotic exposure during neonatal age can modify neuronal development in sensitive subjects (2,3). Nutri-epigenomics studies the impact of micro- and macro-nutrients on gene expression; functional groups (i.e. methyl, acetyl, phosphate, etc) deriving from food oxidation can link with aminoacidic residues at histone tails modify chromatin structure. Furthermore, cytosine methylation at CpG island can modulate gene expression and inhibits transposon mobility, resulting in a proper functionality and genome stability. Studies on experimental models highlight that high fat or low protein diet can lead to disease development in exposed parents and in their offspring due to epigenetic changes; disease can be controlled inhibiting epigenetic inheritance linked to the observed disorder (4). Epigenetic biomarkers (i.e. RXRA) at umbilical cord tissue have been identified and correlated to the increased susceptibility to obesity in adolescents and other diseases at adult age (5). Referenze 1. Tobi EW et al., Human Molecular Genetics, 2009;18 (21): 4046-4053 2. Bordoni L, Gabbianelli R. Biochimie 2019; 160:156-171. 3. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 4. Guida MC et al., Nature Communications (2019)10:193 | https://doi.org/10.1038/s41467-018-08128-3. 5. Godfrey KM, et al. Diabetes. 2011;60(5):1528–1534. doi:10.2337/db10-0979.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
