Abstract
Choline dietary intake varies such that many people do not achieve adequate intakes. Diet intake of choline can modulate methylation because, via betaine homocysteine methyltransferase (BHMT), this nutrient (and its metabolite, betaine) regulate the concentrations of S-adenosylhomocysteine and S-adenosylmethionine. Some of the epigenetic mechanisms that modify gene expression without modifying the genetic code depend on the methylation of DNA or of histones; and diet availability of choline and other methyl-group donors influences both of these methylations. Examples of methyl-donor mediated epigenetic effects include the changes in coat color and body weight in offspring when pregnant agouti mice are fed high choline, high methyl diets; the changes in tail kinking in offspring when pregnant Axin(Fu) mice are fed high choline, high methyl diets; the changes in Cdkn3 methylation and altered brain development that occurs in offspring when pregnant rodents are fed low choline diets. When choline metabolism is disrupted by deleting the gene Bhmt, DNA methylation is affected (especially in a region of chromosome 13), expression of specific genes is suppressed, and liver cancers develop. Better understanding of how nutrients such as choline and methyl-donors influence epigenetic programs has importance for our understanding of not only developmental abnormalities but also for understanding the origins of chronic diseases.
Highlights
Our genetic code is the same in almost every cell in our body, yet all tissues do not express every gene to the same extent
Genome-wide epigenetic status is established in early life with different cell types developing different epigenetic programs that are usually maintained throughout later life
The dietary choline-mediated effects on epigenetic marks are not limited to the genes discussed above; feeding pregnant mice a diet low in choline decreased cytosine methylation in the gene cyclin dependent kinase 3 (Cdkn3), resulting in increased expression of this gene that inhibits cell cycling [43]
Summary
Our genetic code is the same in almost every cell in our body, yet all tissues do not express every gene to the same extent. This difference between tissues occurs because there are epigenetic mechanisms that modify gene expression without modifying the genetic code [1,2,3]. This is fortunate because it permits retuning of gene expression to achieve some degree of adaptation to the environment, including the nutrition environment. Genome-wide epigenetic status is established in early life with different cell types developing different epigenetic programs that are usually maintained throughout later life. Gene expression retuning in early life can affect metabolism and organ function in later life
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
