Vitamins and Carcinogenesis Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Proc Nutr Soc. 2012 Feb;71(1):75-83. doi: 10.1017/S0029665111003302. Epub 2011 Nov 4.
Nutritional epigenetics has emerged as a novel mechanism underlying gene-diet interactions, further elucidating the modulatory role of nutrition in aging and age-related disease development. Epigenetics is defined as a heritable modification to the DNA that regulates chromosome architecture and modulates gene expression without changes in the underlying bp sequence, ultimately determining phenotype from genotype. DNA methylation and post-translational histone modifications are classical levels of epigenetic regulation. Epigenetic phenomena are critical from embryonic development through the aging process, with aberrations in epigenetic patterns emerging as aetiological mechanisms in many age-related diseases such as cancer, CVD and neurodegenerative disorders. Nutrients can act as the source of epigenetic modifications and can regulate the placement of these modifications. Nutrients involved in one-carbon metabolism, namely folate, vitamin B12, vitamin B6, riboflavin, methionine, choline and betaine, are involved in DNA methylation by regulating levels of the universal methyl donor S-adenosylmethionine and methyltransferase inhibitor S-adenosylhomocysteine. Other nutrients and bioactive food components such as retinoic acid, resveratrol, curcumin, sulforaphane and tea polyphenols can modulate epigenetic patterns by altering the levels of S-adenosylmethionine and S-adenosylhomocysteine or directing the enzymes that catalyse DNA methylation and histone modifications. Aging and age-related diseases are associated with profound changes in epigenetic patterns, though it is not yet known whether these changes are programmatic or stochastic in nature. Future work in this field seeks to characterise the epigenetic pattern of healthy aging to ultimately identify nutritional measures to achieve this pattern.
营养表观遗传学已成为基因-饮食相互作用的一种新机制，进一步阐明了营养在衰老和与年龄相关的疾病发展中的调节作用。表观遗传学被定义为 DNA 的一种可遗传修饰，它调节染色体结构并调节基因表达，而不会改变潜在的碱基对序列，最终从基因型决定表型。DNA 甲基化和翻译后组蛋白修饰是经典的表观遗传调控水平。表观遗传现象从胚胎发育到衰老过程中都至关重要，表观遗传模式的异常是许多与年龄相关的疾病（如癌症、心血管疾病和神经退行性疾病）的病因机制。营养素可以作为表观遗传修饰的来源，并可以调节这些修饰的位置。一碳代谢中涉及的营养素，即叶酸、维生素 B12、维生素 B6、核黄素、蛋氨酸、胆碱和甜菜碱，通过调节通用甲基供体 S-腺苷甲硫氨酸和甲基转移酶抑制剂 S-腺苷同型半胱氨酸的水平来参与 DNA 甲基化。其他营养素和生物活性食物成分，如视黄酸、白藜芦醇、姜黄素、萝卜硫素和茶多酚，可以通过改变 S-腺苷甲硫氨酸和 S-腺苷同型半胱氨酸的水平或指导催化 DNA 甲基化和组蛋白修饰的酶来调节表观遗传模式。衰老和与年龄相关的疾病与表观遗传模式的深刻变化有关，但目前尚不清楚这些变化是程序性的还是随机的。该领域的未来工作旨在描述健康衰老的表观遗传模式，最终确定实现这种模式的营养措施。
