Obesity is a multifactorial disease that depends on the interaction between life style, genetics and the environment. The quantity and quality of food modulate the epigenome throughout life; however, food exerts its maximum epigenetic modulation during cell programming which occurs in the prenatal and early postnatal age of life. During this period, several environmental factors can modify the epigenetic signature perturbing gene expression later in life. In fact, although epigenetics can be reversed, the epigenetic impact of environmental factors (e.g. food intake, life style) during cell programming produces stable modifications which are maintained across the lifetime, modifying gene expression and promoting the development of several diseases (e.g. obesity, glucose intolerance, cardiovascular diseases, neurodegeneration) (1,2). In particular, malnutrition, denoting as either excess or reduced nutrients intake, and the exposure to xenobiotics, can modulate the epigenome and gut microbiota metabolite production, leading to changes that can be associated with the development of an obese phenotype (2,3). The modulatory activity of functional groups obtained from food during early life has been observed in several organisms, and its characterization highlights the key role of epigenetics in satiety regulation or food intake. The quality of food can also have an impact on obesity across life and can impact future generations as demonstrated by several studies on epigenetic modulation of endocrine disrupting chemicals (EDCs) (4-6). EDCs contained in food or released from food contact materials, promote an increase in body weight affecting adipogenesis, lipid accumulation, inflammation, metabolic syndrome development and gut microbiota (5). Finally, obese phenotype development also depends on the individual genetic variability which modulates the responses to food intake, environment and EDCs (2). Keywords: Nutri-epigenomics; obesity; endocrine disrupting chemicals. References 1. Gabbianelli R, Damiani E. Epigenetics and neurodegeneration: role of early-life nutrition. J Nutr Biochem. 2018; 57:1-13. doi: 10.1016/j.jnutbio.2018.01.014. 2. Bordoni L, Gabbianelli R. Primers on nutrigenetics and nutri(epi)genomics: Origins and development of precision nutrition. Biochimie. 2019; 160:156-171. doi: 10.1016/j.biochi.2019.03.006. 3. Li Y Epigenetic Mechanisms Link Maternal Diets and Gut Microbiome to Obesity in the Offspring. 2018; Front. Genet. 9:342. doi: 10.3389/fgene.2018.00342 4. Skinner MK, Manikkam M, Tracey R, Guerrero-Bosagna C, Haque M, Nilsson EE. 2013. Ancestral dichlorodiphenyltrichloroethane (DDT) exposure promotes epigenetic transgenerational inheritance of obesity. BMC Med 11 228, doi:10.1186/1741-7015-11-228 5. Petrakis D, Vassilopoulou L, Mamoulakis C, et al. Endocrine Disruptors Leading to Obesity and Related Diseases. Int J Environ Res Public Health. 2017; 14(10): 1282. doi:10.3390/ijerph14101282 6. Mantovani A. Endocrine Disrupters and the Safety of Food Chains. Horm Res Paediatr. 2016; 86(4):279-288. .

Nutri-epigenetics and nutri-epigenomics

Rosita Gabbianelli
2019

Abstract

Obesity is a multifactorial disease that depends on the interaction between life style, genetics and the environment. The quantity and quality of food modulate the epigenome throughout life; however, food exerts its maximum epigenetic modulation during cell programming which occurs in the prenatal and early postnatal age of life. During this period, several environmental factors can modify the epigenetic signature perturbing gene expression later in life. In fact, although epigenetics can be reversed, the epigenetic impact of environmental factors (e.g. food intake, life style) during cell programming produces stable modifications which are maintained across the lifetime, modifying gene expression and promoting the development of several diseases (e.g. obesity, glucose intolerance, cardiovascular diseases, neurodegeneration) (1,2). In particular, malnutrition, denoting as either excess or reduced nutrients intake, and the exposure to xenobiotics, can modulate the epigenome and gut microbiota metabolite production, leading to changes that can be associated with the development of an obese phenotype (2,3). The modulatory activity of functional groups obtained from food during early life has been observed in several organisms, and its characterization highlights the key role of epigenetics in satiety regulation or food intake. The quality of food can also have an impact on obesity across life and can impact future generations as demonstrated by several studies on epigenetic modulation of endocrine disrupting chemicals (EDCs) (4-6). EDCs contained in food or released from food contact materials, promote an increase in body weight affecting adipogenesis, lipid accumulation, inflammation, metabolic syndrome development and gut microbiota (5). Finally, obese phenotype development also depends on the individual genetic variability which modulates the responses to food intake, environment and EDCs (2). Keywords: Nutri-epigenomics; obesity; endocrine disrupting chemicals. References 1. Gabbianelli R, Damiani E. Epigenetics and neurodegeneration: role of early-life nutrition. J Nutr Biochem. 2018; 57:1-13. doi: 10.1016/j.jnutbio.2018.01.014. 2. Bordoni L, Gabbianelli R. Primers on nutrigenetics and nutri(epi)genomics: Origins and development of precision nutrition. Biochimie. 2019; 160:156-171. doi: 10.1016/j.biochi.2019.03.006. 3. Li Y Epigenetic Mechanisms Link Maternal Diets and Gut Microbiome to Obesity in the Offspring. 2018; Front. Genet. 9:342. doi: 10.3389/fgene.2018.00342 4. Skinner MK, Manikkam M, Tracey R, Guerrero-Bosagna C, Haque M, Nilsson EE. 2013. Ancestral dichlorodiphenyltrichloroethane (DDT) exposure promotes epigenetic transgenerational inheritance of obesity. BMC Med 11 228, doi:10.1186/1741-7015-11-228 5. Petrakis D, Vassilopoulou L, Mamoulakis C, et al. Endocrine Disruptors Leading to Obesity and Related Diseases. Int J Environ Res Public Health. 2017; 14(10): 1282. doi:10.3390/ijerph14101282 6. Mantovani A. Endocrine Disrupters and the Safety of Food Chains. Horm Res Paediatr. 2016; 86(4):279-288. .
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11581/430060
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