表觀(guān)遺傳學(xué)修飾可以不改變基因編碼,，而影響基因的開(kāi)啟或關(guān)閉,。研究人員對(duì)185位志愿者（84位男性和101位女性）的直腸組織切片進(jìn)行了研究，發(fā)現(xiàn)人體內(nèi)基因的表觀(guān)遺傳學(xué)修飾主要受衰老的驅(qū)動(dòng),，不過(guò)日常飲食也會(huì)對(duì)表觀(guān)遺傳學(xué)修飾產(chǎn)生重要影響,。該研究發(fā)表在十二月六日的Aging Cell雜志上。
研究顯示年齡對(duì)表觀(guān)遺傳學(xué)修飾影響最大,，同時(shí)人體內(nèi)的硒和維生素D可以減少表觀(guān)遺傳學(xué)修飾的累積,，而血液中高含量的葉酸和肥胖則會(huì)增加表觀(guān)遺傳學(xué)修飾的水平。說(shuō)明日常飲食健康衰老有重要影響,。
英國(guó)食品研究所的Nigel Belshaw領(lǐng)導(dǎo)研究人員,，對(duì)進(jìn)行臨床結(jié)腸鏡檢查的志愿者進(jìn)行了研究，檢測(cè)了他們的腸壁細(xì)胞,。這些志愿者沒(méi)有患癌癥或炎癥性腸病,，也沒(méi)有在日常飲食以外補(bǔ)充其他營(yíng)養(yǎng)物。研究人員在上述志愿者的基因中尋找與腸癌相關(guān)的表觀(guān)遺傳學(xué)修飾（DNA甲基化）,，腸癌是衰老相關(guān)的癌癥,。甲基化標(biāo)志可以隨著細(xì)胞分裂而傳遞，不少甲基化修飾都與癌癥發(fā)展有關(guān),。
研究人員針對(duì)上述癌癥相關(guān)表觀(guān)遺傳學(xué)修飾與志愿者自身因素（包括年齡,、性別、體形以及血液中一些營(yíng)養(yǎng)物質(zhì)的水平）之間的關(guān)聯(lián)進(jìn)行了研究,。結(jié)果顯示,，對(duì)基因甲基化影響最大的是年齡。與此相符,，腸癌的最大風(fēng)險(xiǎn)因子就是年齡,，五十歲以上患病風(fēng)險(xiǎn)呈指數(shù)增長(zhǎng),。
研究還指出，男性表觀(guān)遺傳學(xué)修飾的頻率比女性高,，這一點(diǎn)與醫(yī)學(xué)常識(shí)一致,，即男性患腸癌的風(fēng)險(xiǎn)更高,。研究人員發(fā)現(xiàn),，維生素D和硒水平較高的志愿者，其腸癌相關(guān)甲基化水平較低,。與此一致的是,，有不少研究表明維生素D和硒水平高可以降低腸癌風(fēng)險(xiǎn)。
葉酸是人體健康所必需的,，但在這項(xiàng)研究中,，葉酸水平高與腸癌相關(guān)表觀(guān)遺傳學(xué)修飾增加聯(lián)系起來(lái)。此前也有一些研究顯示,，過(guò)量葉酸攝入可能使一些人得腸癌的風(fēng)險(xiǎn)增加,。近來(lái)還有研究指出，在體外培養(yǎng)的細(xì)胞中,，高葉酸水平會(huì)促使這些表觀(guān)遺傳學(xué)修飾發(fā)生,。這些研究都強(qiáng)調(diào)，人們需要進(jìn)一步研究來(lái)確定人體內(nèi)的最佳葉酸水平,。研究人員也將在隨后的研究中分析葉酸對(duì)DNA甲基化的具體影響,。
肥胖也是腸癌的風(fēng)險(xiǎn)因子之一，研究人員發(fā)現(xiàn)人的體形（身高,、體重和腰圍）與表觀(guān)遺傳學(xué)修飾有?，F(xiàn)在研究人員正在評(píng)估體重對(duì)于表觀(guān)遺傳學(xué)修飾和腸道健康有何影響,。
總的來(lái)說(shuō),，這項(xiàng)研究指出衰老能夠影響一些基因的表觀(guān)遺傳學(xué)修飾水平，而這類(lèi)影響受到飲食和肥胖程度的調(diào)解,。(生物谷Bioon.com)
DOI: 10.1111/acel.12030
PMC:
PMID:
Nutritional factors and gender influence age-related DNA methylation in the human rectal mucosa
Henri S. Tapp1, Daniel M. Commane2, D. Michael Bradburn3, Ramesh Arasaradnam2, John C. Mathers2, Ian T. Johnson1, Nigel J. Belshaw1,*
Aberrant methylation of CpG islands (CGI) occurs in many genes expressed in colonic epithelial cells, and may contribute to the dysregulation of signalling pathways associated with carcinogenesis. This cross-sectional study assessed the relative importance of age, nutritional exposures and other environmental factors in the development of CGI methylation. Rectal biopsies were obtained from 185 individuals (84 male, 101 female) shown to be free of colorectal disease, and for whom measurements of age, body size, nutritional status and blood cell counts were available. We used quantitative DNA methylation analysis combined with multivariate modelling to investigate the relationships between nutritional, anthropometric and metabolic factors and the CGI methylation of 11 genes, together with LINE-1 as an index of global DNA methylation. Age was a consistent predictor of CGI methylation for 9/11 genes but significant positive associations with folate status and negative associations with vitamin D and selenium status were also identified for several genes. There was evidence for positive associations with blood monocyte levels and anthropometric factors for some genes. In general, CGI methylation was higher in males than in females and differential effects of age and other factors on methylation in males and females were identified. In conclusion, levels of age-related CGI methylation in the healthy human rectal mucosa are influenced by gender, the availability of folate, vitamin D and selenium, and perhaps by factors related to systemic inflammation.
