Genetic-Epigenetic Nutrition ma lo tatou Soifua Maloloina | El Paso, TX.
E fa'afefea ona saofagā le epigenetic ma mea'ai fa'apitoa mo le soifua maloloina lelei?
O le to'atele oi tatou e iloa mea'ai le lelei e a'afia ai o tatou tino. latou
- Faagesegese le Metabolism
- Faaopoopo le Mamafa
- Fa'apala ma fa'ama'a'a ala ma isi.
Ae o lea ua iai meaʻai ma meaʻai e mafai ona fesoasoani ia i tatou i se auala ma e sau mai se nofoaga tatou te le mafaufau i ai, ma o lo tatou DNA lena.
Nutriepigenomics e suʻesuʻeina fesoʻotaʻiga i le va o meaʻai ma biomarkers e mafai ona faʻapipiʻi pe aveese mai a tatou DNA. O le mea lea e liliu ai a tatou kenera i luga pe tape.
O suʻesuʻega fou o loʻo faʻaalia ai le mautinoa mea'ai po'o mea fa'aopoopo e mafai ona fetuutuunai le faailoaga o o tatou kenera, lea e mafai ona aafia ai lo tatou soifua maloloina.
Nutritional genomics o lo'o fa'afouina faiga fa'alesoifua maloloina ma le soifua maloloina lautele:
Mea'ai, fa'amalositino, ma le fa'aalia o le si'osi'omaga o elemene uma ia na fa'aalia ai se sao i le fesuia'iina o kenera i luga ma tape ese e ala i epigenetics. O le fetuutuuna'i o tulaga o le olaga e mafai ona pulea ai le gafatia e fa'aitiitia ai fa'ama'i ma iai se aafiaga lelei i lo tatou soifua maloloina.
Soifua Maloloina mai i itu uma ua amata ona faʻapipiʻi epigenetics i totonu o latou faʻataʻitaʻiga faʻamoemoe e tuʻuina atu fuafuaga faʻapitoa ma faʻapitoa mo togafitiga.
"O le faʻapipiʻiina o faʻamatalaga e pei o meaʻai, olaga, mea tau le siosiomaga, talaʻaga o aiga, faʻamaoniga, ma suʻesuʻega faʻatasi ai ma epigenetics e mafai ona fesoasoani e taʻitaʻia ai se tasi i se tulaga o le soifua maloloina lelei," o le tala lea a Kristy Hall, MS, RNCP, ROHP, o se komiti faʻamaonia o meaʻai taumafa ma na faavaeina le Living Well Nutrition o loʻo faʻaaogaina suʻega epigenetic, faufautua tau meaʻai, ma se auala faʻapitoa e sili atu ona saunia mo ana tagata faʻatau.
Ia 15, 2018, Bailey Kirkpatrick meaʻai, Fa'ama'i & Fa'aletonu, siosiomaga, Tala Fou & Faʻamatalaga
O lo'o i ai le avanoa o tagata su'esu'e i mea'ai ua resitalaina e faia ai fautuaga fa'amea'ai e fa'atatau i mea'ai e mafai ona fa'aleleia atili ai le soifua maloloina o tagata.
O mea'ai o se tasi lea o mea taua o le siosiomaga e fuafua ai lo tatou soifua maloloina. O fa'ama'i tumau e aofia ai:
- Tusia le maʻisuka 2
- Metabolic syndrome
- Paʻi cardiovascular
- Fa'ama'i fa'ama'i
- Vaʻaia eseese
- E amataina pe faatelevaveina e mea'ai/mea'ai
Ole vaega ole su'esu'ega tau mea'ai e mafai ona ta'ua ole Nutritional Genomics.
Nucleotide polymorphisms tasi (SNPs) o eseesega faavae-paiga tasi i le DNA. Latou te fai ma sui o se ituaiga autu o fesuiaiga o kenera tagata.
O le mole mole DNA pito i luga e ese mai le mole DNA pito i lalo i se nofoaga e tasi (se C/A polymorphism)
Nutritional genetics poʻo nutrigenetics e aofia ai le fa'ailoaina, fa'avasegaga, ma fa'ailoga o suiga ole kenera a le tagata lea e suia ai le metabolism/fa'aogaina o mea'ai ma fa'apalepale mea'ai Ata1.
Fa'aoga: Genetic & Epigenetics
Nutrient, mo se faataitaiga, Foma'i, o ni aafiaga mamana o le genome expression ma le mautu, ma o nei kene-nutrient fegalegaleaiga e mafai ona sili ona lelei mo le puipuia o faʻamaʻi.
Mea'ai Ta'ito'atasi
O lo'o fa'aauau pea le folafolaga mo le soifua maloloina lelei e ala i taumafa, ae o lo'o fa'atumauina e le mamalu o le atunu'u ni fa'amoemoega lelei, e pei ona molimauina i le fa'aogaina o mea'ai fa'aopoopo.
O su'esu'ega fa'asaienisi o lo'o fa'aalia ai o mea'ai i mea'ai eseese ma mea'ai fa'aopoopo tatou te 'ai e ono mafai ona fetu'una'i pe toe fa'afo'i suiga fa'atosina. O lenei faʻamaoniga e mafai ona faʻaaogaina i le faia o filifiliga sili atu o le olaga.
Blueberries e matua maualuga lava i antioxidants ma e manatu o lenei 'superfood' e mafai ona faʻaitiitia ai le faaleagaina o le DNA, ma puipuia ai tagata mai le kanesa ma atonu e faʻagesegese ai le matua. O le sua o le Blueberry ma le vaitamini C ua faʻaalia e mafai ona avea ma inhibitors methylation mo le MTHFR gene ma le DNMT1 gene i tagata.
Kim, M., Na, H., Kasai, H., Kawai, K., Li, Y.-S., & Yang, M. (2017). Fa'atusatusaga ole Blueberry (Vaccinium spp.) ma Vitamini C e ala ile Antioxidative and Epigenetic Effects in Human. Tusitala o le Puipuiga o le Kanesa, 22(3), 174–181.
O le aʻoaʻoina o mea tatou te 'ai ma mea e fai i o tatou tino, aemaise lava aʻafiaga epigenetic, e naʻo le tasi le laʻasaga latalata i le soifua maloloina lelei.
O le tele o mea taua, faʻamaʻi tele, ma malamalama atili i auala e faʻavae ai fegalegaleaiga i le va o le soifuaga, siosiomaga, ma genetics e taua tele mo le atinaʻeina o fuafuaga lelei mo le puipuiga ma togafitiga [1].
Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into�the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.
(i) Suiga o le Epigenetic i le Atinaʻe Faʻatasi ma Meaʻai Fafaga I le taimi o le Gestation
Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13�15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes,�especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20�30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic �memory� response that precedes development of the altered phenotype in offspring.
Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31�34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling [35]. Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.
O le faʻaaogaina o faʻamaumauga o le epigenetic i le tele o augatupulaga e lelei ona faʻamatalaina i faʻalaʻau laau ma C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species [31]. The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse [38]. In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation�mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color [41]. One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 [42]; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.
E ui o le tele o suʻesuʻega ua faʻamalamalamaina suiga o le epigenetone i meaʻai, e faʻaaoga ai le faʻaaogaina o nofoaga faʻataʻatia a le au faipisinisi, o loʻo i ai ni nai suʻesuega lautele na faia. O se suʻesuʻega talu ai nei sa taulaʻi i le fuafuaina o le epigenethera faʻasolosolo o mea taumafa maualuga / taumafa-meaʻai i totonu o tamaʻi matutua e faʻaaoga ai genome-wide generic expression ma DNA methylation analyzes [43]. O lenei suʻesuʻega na faʻaalia ai 232 faʻapitoa methylated eria (DMRs) i adipocytes mai le pulea ma le maualuga-gaʻo fafagaina o nifo. O le mea sili ona taua, o vaega tutusa o tagata mo le DMR misa sa ese foi le methylated i le tino o le tino mai le faitau aofaʻi o tagata maualuluga ma vaivai, ma ua faʻamaonia ai le maoae o le faʻasaoina o nei vaipanoa. O lenei taunuʻuga e faʻamalosia ai le taua o le DMR ua faʻamaonia i le faʻatonutonuina o le malosiaga o le homeostasis i mamame.
(i) Suʻesuʻega faʻatalanoaga faʻatasi. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential�methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46�48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation [49].
Mai nei suʻesuʻega, o le methylation fesuiaiga o le PGC1A, HIF3A, ABCG1, ma le CPT1A ma le RXRA [18] na faʻamatalaina talu ai nei na faʻaalia mai o ni tagata e ola faʻatasi ma, pe atonu foi o le, o le soifua maloloina ole soifua maloloina e avea ma sui talafeagai mo le atiina ae o faamai pipisi. .
Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20�40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping�with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 [8]. Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice [43] and weight loss in humans [64]. These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.
Tausaga faʻapitoa: Two recently published studies made use of human populations that experienced �natural� variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants [69]. The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood [68]. The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.
Siosiomaga Faʻasalalauga: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the �mature� epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells [77], and muscle tissue [78] in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver [79] and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat [64]. Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80�82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport [83]. Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss [84].
DNA methylation suiga e fesoʻotaʻi ma le lapoʻa pe faʻatosinaina e le taumafataga poʻo ituaiga olaga ma le paʻu o pauna e masani ona tauagafau (<15%), e ui o lenei e fesuisuiaʻi faʻalagolago i le phenotype ma le tino na suʻesuʻeina. Mo se faʻataʻitaʻiga, o suiga e sili atu nai lo le 20% ua lipotia mai i le adipose tissue ina ua maeʻa le paʻu o le mamafa [64] ma fegalegaleaiga i le va o le HIF3A methylation ma le BMI i le adipose tissue na sili atu ona taua nai lo le toto [52].
faaiuga
