Diet is one of the main factors that can impact gene expression and gut microbiota diversity and it provides the functional groups required for epigenome modulation. Starting from early life, the exposome (e.g. diet, xenobiotics, drugs, etc.) is responsible for specific epigenetics marks [1,2]. A maternal high fat diet and food pesticide exposure during the pre- and post-natal period of live can promote inflammatory responses in offspring that may influence organ development promoting a healthy/unhealthy phenotype in adulthood. High protein and carbohydrate (e.g. fructose, glucose) intake in adult age can play a key role in the development of chronic low-grade systemic inflammation [3]. Of particular concern is that epigenetic marks of diseases may be inherited, hence they can mediate epigenetic inheritance of diseases [4,5]. In this context, nutrigenomics mediated by bioactive compounds and a balanced nutrient intake can actively control inflammation and maintain the cellular redox homeostasis. A summary of data on how and when nutrigenomics can modulate inflammatory responses through healthy dietary choices to prevent the main inflammatory-related metabolic diseases occurring across life will be presented. References 1. Gabbianelli R, Damiani E. J Nutr Biochem. 2018; 57:1-13. 2. Bordoni L, Gabbianelli R. Biochimie. 2019; 160:156-171. 3. Yamashita A.S. et al., Mediators of Inflammation 2018; Article ID 8261432. 4. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 5. Sun W et al. Adv Sci (Weinh). 2019;16;6(11):1900275.
Nutrigenomics and inflammation
Gabbianelli R
2019-01-01
Abstract
Diet is one of the main factors that can impact gene expression and gut microbiota diversity and it provides the functional groups required for epigenome modulation. Starting from early life, the exposome (e.g. diet, xenobiotics, drugs, etc.) is responsible for specific epigenetics marks [1,2]. A maternal high fat diet and food pesticide exposure during the pre- and post-natal period of live can promote inflammatory responses in offspring that may influence organ development promoting a healthy/unhealthy phenotype in adulthood. High protein and carbohydrate (e.g. fructose, glucose) intake in adult age can play a key role in the development of chronic low-grade systemic inflammation [3]. Of particular concern is that epigenetic marks of diseases may be inherited, hence they can mediate epigenetic inheritance of diseases [4,5]. In this context, nutrigenomics mediated by bioactive compounds and a balanced nutrient intake can actively control inflammation and maintain the cellular redox homeostasis. A summary of data on how and when nutrigenomics can modulate inflammatory responses through healthy dietary choices to prevent the main inflammatory-related metabolic diseases occurring across life will be presented. References 1. Gabbianelli R, Damiani E. J Nutr Biochem. 2018; 57:1-13. 2. Bordoni L, Gabbianelli R. Biochimie. 2019; 160:156-171. 3. Yamashita A.S. et al., Mediators of Inflammation 2018; Article ID 8261432. 4. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 5. Sun W et al. Adv Sci (Weinh). 2019;16;6(11):1900275.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
