The role of vitamins and minerals in modulating the expression of microRNA

Beckett, Emma L.; Yates, Zoë; Veysey, Martin; Duesing, Konsta; Lucock, Mark

doi:10.1017/s0954422414000043

Cited by 53 publications

(41 citation statements)

References 163 publications

(197 reference statements)

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“…There is some evidence that endogenous miRNAs in different bodily compartments are modulated by dietary factors, such as glucose, vitamins, trace elements, drugs, or simply intake of food in general [52–54]. This modulation might occur through miRNA regulation in cells and/or by differential release from cells exposed to dietary components.…”

Section: Dependence On Various Forms Of Self-reports Of Dietary Intakmentioning

confidence: 99%

Diet-derived microRNAs: unicorn or silver bullet?

Witwer

Zhang

2017

Genes Nutr

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In ancient lore, a bullet cast from silver is the only effective weapon against monsters. The uptake of active diet-derived microRNAs (miRNAs) in consumers may be the silver bullet long sought after in nutrition and oral therapeutics. However, the majority of scientists consider the transfer and regulation of consumer’s gene activity by these diet-derived miRNAs to be a fantasy akin to spotting a unicorn. Nevertheless, groups like Dr. Chen-Yu Zhang’s lab in Nanjing University have stockpiled breathtaking amounts of data to shoot down these naysayers. Meanwhile, Dr. Ken Witwer at John Hopkins has steadfastly cautioned the field to beware of fallacies caused by contamination, technical artifacts, and confirmation bias. Here, Dr. Witwer and Dr. Zhang share their realities of dietary miRNAs by answering five questions related to this controversial field.

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Section: Dependence On Various Forms Of Self-reports Of Dietary Intakmentioning

confidence: 99%

Diet-derived microRNAs: unicorn or silver bullet?

Witwer

Zhang

2017

Genes Nutr

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“…Genomic methylation is a critical process in facilitating gene regulation, with mounting evidence suggesting that micronutrients play an important role in many epigenetic phenomena [29] , not just the obvious role that folate, methionine and vitamin B12 in particular play in facilitating methyl group transfer, but in wider phenomena such as microRNA occurrence/function [29] . The link between relevant aspects of one-carbon metabolism and colon pathoaetiology is compelling, and the present data provide valuable new information linking diet to the development of AP.…”

Section: Discussionmentioning

confidence: 99%

Methylation diet and methyl group genetics in risk for adenomatous polyp occurrence

Lucock¹,

Yates²,

Martin³

et al. 2015

BBA Clinical

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PurposeThe aim of this study is to explore whether a methylation diet influences risk for adenomatous polyps (AP) either independently, or interactively with one-carbon metabolism-dependent gene variants, and whether such a diet modifies blood homocysteine, a biochemical phenotype closely related to the phenomenon of methylation.Methods249 subjects were examined using selective fluorescence, PCR and food frequency questionnaire to determine homocysteine, nine methylation-related gene polymorphisms, dietary methionine, 5-methyltetrahydrofolate, vitamins B6 and B12.Results1). Both dietary methionine and 5-methyltetrahydrofolate intake are significantly associated with plasma homocysteine. 2). Dietary methionine is related to AP risk in 2R3R-TS wildtype subjects, while dietary B12 is similarly related to this phenotype in individuals heterozygous for C1420T-SHMT, A2756G-MS and 844ins68-CBS, and in those recessive for 2R3R-TS. 3). Dietary methionine has a marginal influence on plasma homocysteine level in C1420T-SHMT heterozygotes, while B6 exhibits the same effect on homocysteine in C776G-TCN2 homozygote recessive subjects. Natural 5-methyltetrahydrofolate intake is interesting: Wildtype A1298C-MTHFR, heterozygote C677T-MTHFR, wildtype A2756G-MS and recessive A66G-MSR individuals all show a significant reciprocal association with homocysteine. 4). Stepwise regression of all genotypes to predict risk for AP indicated A2756G-MS and A66G-MSR to be most relevant (p = 0.0176 and 0.0408 respectively). Results were corrected for age and gender.ConclusionA methylation diet influences methyl group synthesis in the regulation of blood homocysteine level, and is modulated by genetic interactions. Methylation-related nutrients also interact with key genes to modify risk of AP, a precursor of colorectal cancer. Independent of diet, two methylation-related genes (A2756G-MS and A66G-MSR) were directly associated with AP occurrence.

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“…16 Nutrients can also modify gene expression indirectly, via modulation of gene regulatory factors such as epigenetic marks, including the involvement of DNA methylation and miRNA. 17 Importantly, nutrigenetics can impact upon the nutrigenomic and epigenetic responses and the sum of these events can modify disease risk. 18 With improving technology, and completion of ground-breaking research, such as the human genome project, we are learning more about gene-nutrient interactions.…”

Section: Gene-nutrient Interactionsmentioning

confidence: 99%

Nutrigenetics—Personalized Nutrition in the Genetic Age

Beckett¹,

Jones²,

Veysey³

et al. 2017

Exploratory Research and Hypothesis in Medicine

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Diet is an important modifiable determinant of disease, and it is becoming clear that diet and genetic risk factors are interactive in determining risk for diseases such as cardiovascular disease, diabetes and cancers. Advances in technology have improved our understanding of gene-nutrient interactions, and lead to the development of nutrigenetics, personalized nutrition based on genetics. While evidence is strong for some associations, others remain unclear. As such, the implementation of nutrigenetics remains controversial. While some argue it is not ready for clinical use, it has also been argued that nutrigenetics is unfairly held to a higher standard than traditional nutrition research. Despite the future promise of nutrigenetic testing for improving health outcomes, several barriers in science, technology, acceptance and ethics exist to its implementation. Gene-nutrient associations have been identified in a number of lifestyle-associated diseases, and better understanding of these relationships may lead to improved health outcomes. However, the success of nutrigenetics is not only dependent on the strength of the science, but in consumer acceptance and uptake. This narrative review provides an overview of the current landscape for nutrigenetics in relation to key disease states, and addresses the potential barriers to implementation.

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The role of vitamins and minerals in modulating the expression of microRNA

Cited by 53 publications

References 163 publications

Diet-derived microRNAs: unicorn or silver bullet?

Diet-derived microRNAs: unicorn or silver bullet?

Methylation diet and methyl group genetics in risk for adenomatous polyp occurrence

Nutrigenetics—Personalized Nutrition in the Genetic Age

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