nutritional exposure during pregnancy could induce epigenetic changes in metabolic tissues of the offspring.
There is increasing evidence that obesity has developmental origins such as, an exposure to a suboptimal nutrient supply before birth or in early infancy is associated with an increased risk of obesity and metabolic disease in later life(McMillen, Adam and Mühlhäusler, 2005; Waterland and Michels, 2007; McMillen et al., 2008). Animals studies have been performed to provide evidence that early life nutritional exposure could induce epigenetic changes in key metabolic tissues of the offspring (Bouret, Levin and Ozanne, 2014; Ge et al., 2014). These changes stay after birth and result in permanent gene alterations during the further life …show more content…
All epigenetic mechanisms are mitotically heritable and may also be meiotically heritable which has the potential for transgenerational epigenetic inheritance. The best example of this epigenetic inheritance in mammals is genomically imprinted genes, which are expressed from either the maternally or paternally inherited allele (Wood & Oakey 2006; Reik & Walter 2001). These imprinted genes are turned off in a parent-of-origin dependent manner. If the allele inherited is paternally imprinted, it is thereby silenced and only the maternal allele is expressed and vice versa(Reik and Walter, 2001). Imprinted expression can also vary between tissues, developmental stages, and species. Imprinted genes are involved in differentiation, development, viability and metabolic functions(Lee et al., 1999). In Lee et al., they demonstrated that two main clusters of genomic imprinting are known in humans: a region at 11p15 containing several imprinted maternally expressed genes like H19, KNCQ1 and paternally expressed genes like IGF2, INS, KCNQ10T1 (LIT1). The second cluster is at 15q11-q12 and contains at least 7 maternally and paternally genes(Schweizer, Zynger and Francke,
There is increasing evidence that obesity has developmental origins such as, an exposure to a suboptimal nutrient supply before birth or in early infancy is associated with an increased risk of obesity and metabolic disease in later life(McMillen, Adam and Mühlhäusler, 2005; Waterland and Michels, 2007; McMillen et al., 2008). Animals studies have been performed to provide evidence that early life nutritional exposure could induce epigenetic changes in key metabolic tissues of the offspring (Bouret, Levin and Ozanne, 2014; Ge et al., 2014). These changes stay after birth and result in permanent gene alterations during the further life …show more content…
All epigenetic mechanisms are mitotically heritable and may also be meiotically heritable which has the potential for transgenerational epigenetic inheritance. The best example of this epigenetic inheritance in mammals is genomically imprinted genes, which are expressed from either the maternally or paternally inherited allele (Wood & Oakey 2006; Reik & Walter 2001). These imprinted genes are turned off in a parent-of-origin dependent manner. If the allele inherited is paternally imprinted, it is thereby silenced and only the maternal allele is expressed and vice versa(Reik and Walter, 2001). Imprinted expression can also vary between tissues, developmental stages, and species. Imprinted genes are involved in differentiation, development, viability and metabolic functions(Lee et al., 1999). In Lee et al., they demonstrated that two main clusters of genomic imprinting are known in humans: a region at 11p15 containing several imprinted maternally expressed genes like H19, KNCQ1 and paternally expressed genes like IGF2, INS, KCNQ10T1 (LIT1). The second cluster is at 15q11-q12 and contains at least 7 maternally and paternally genes(Schweizer, Zynger and Francke,