Tenduristiya Genetîk-Epigenetic û Xweseriya me | El Paso, TX
Tenduristî û xwarinê kesane çawa dihatin tendurustiya herî baş?
Piraniya me di derbarê xwarinên bêhêzî de bizanin ka çawa cesareta me dike? Ew
- Çepê Metabolîzmê
- Weight Add
- Pevçûn û hişk
Lê niha nuha xwarin û elementên xwarin hene ku dikare di rê de alîkarî bikin û ji cîhê ku em ne ji ramana me, û ew DNA e, tê.
Nutriepigenomics têkiliyên di navbera xwarin û biogarkeran de lêkolîn dikin ku ji DNA ve girêdayî an vebirinê vekin. Ev cinsên xwe li ser an jî veguherîne.
Lêkolînên nû têne nîşandan xwarin an xwarinê dikare têgezkirina jenên me, ku dikare tenduristiya xwe bandor bike.
Genomeya giyanî têkoşîna hemî dermanên klînîk û gelemperî tedbîra tenduristiyê dike:
Diet, xebitandinê, û pêşniyara hawirdorê her tiştên ku di jîndanê de guherînan de li ser û zîndanê re rolek nîşan da. Hêzên faktorên lênêrîna karûbarên lênêrînê dikare dikare potansîyona ku nexweşiya kêm bikin û bandorek erênî li ser tendurustiya me heye.
Pisporên tendurustî Ji hemûyan ve dest pê dike ku epigenetics bi karanîna armancên xwe vebikin ku planên bêhtir taybetmendî û takekesî pêşkêş dikin.
Kristy Hall, MS, RNCP, ROHP, pisporê xurekiya fonksiyonel û pejirandî ya lijneyê, got: �Agahiyên qat ên wekî parêz, şêwaza jiyanê, faktorên hawîrdorê, dîroka malbatê, nîşanan, û teşhîs ligel epigenetîk dikare bibe alîkar ku kesek berbi rewşek tenduristiya xweşbîn ve bibe alîkar. damezrînerê Living Well Nutrition ku ceribandina epigenetîk, şêwirmendiya xurek, û nêzîkatiyek piralî bikar tîne da ku ji xerîdarên xwe çêtir peyda bike.
Bila 15, 2018, Bailey Kirkpatrick Parêz, Nexweşî & Bêserûberî, Dor, Nûçe & Nirxandin
Xwarinên qeydkirî hene ku derfetên ku genetîkî bi pêşniyarên xwarinê ve girêdayî ye ku dikare tendurustiya mirovî çêtir bikin.
Xurek ji hêla faktorên hawirdora yekem e ku tendurustiya me diyar dike. Nexweşiyên demjimêr hene
- Tîpa 2 diyabetê
- Syndrome Metabolic
- Nexweşiya cardiovascular
- Nexweşiya neurolojî
- Kanserên Gelek
- Bi xwarinê / xwarinê ve hatî destpêkirin an zûtir kirin
Ev qada lêkolînê ya nutritional dikare dikare wekî wekî Gen Genomics Nerastkirin.
Polymorphîzma yek nucleotide (SNPs) DNA di nav DNA-yekane de cudahiyên yekane-yek in. Ew nûneriya bingehîn ya guhertina genetîkî nîşan dide.
Molekuliya DNA ya ji molekola DNA-yê de li cihê yekane-bayek yekane (cudahî pirrjimaroka C / A)
Genetîk û nutrigeneticsên xwarinî hene nasnameyê, kategoriyê, û taybetmendiyê guhertina genetîkî ya ku metabolîzma nutriyalîzmê / karanîna û tengahîkirina xwarinên Fig1 biguherîne.
Serlêdan: Jenetîk & Epîgenetîk
Nutriyan, wek nimûne, Dermanan, bandorên hêzdar ên genenîf û gihengiya genome hene, û têkiliyên van gene-nutrient dikare ji bo pêşîlêgirtina nexweşî.
Nutrition
Sozdariya endezyariyê ya ji bo tendurustiya herî baş hîn jî berdewam dike, lê gelî hêviyên erênî ye, wekî ku ji hêla bikaranîna xwarinên diranan.
Lêkolînek zanistî nîşan dide ku nutriyan di xwarinên cûda û xwarinên ku em bixwin, dibe ku dibe ku biguhere guhertinên xwe yên xweş bikin. Ev belgeyên ku di hilbijartinên jiyanê de çêtirîn çêtirîn bikar bînin.
Bûz di nav antîoksîdan de pir zêde ye û tê fikirîn ku ev "superxwarin" dikare bi epigenetîk zirara DNA kêm bike, bi vî rengî mirovan li dijî penceşêrê diparêze û dibe ku pîrbûnê jî hêdî bike. Ava şîn û vîtamîna C ji bo gena MTHFR û gena DNMT1 di mirovan de wekî astengkerên metilasyonê yên potansiyel hatine destnîşan kirin.
Kim, M., Na, H., Kasai, H., Kawai, K., Li, Y.-S., & Yang, M. (2017). Berawirdkirina Blueberry (Vaccinium spp.) û Vîtamîn C bi Bandorên Antîoxidative û Epigenetîk ên Di Mirovan de. Kovara Pêşîlêgirtina Penceşêrê, 22 (3), 174-181.
Em di derbarê ku em dixwin û çi dike, ew bedena me dike, bi taybetî bi potansiyona epigenetîk potansî, tenê yek pêngavek nêziktirîn tendurustiya herî baş e.
Qelewbûn nexweşiyek tevlihev, pir-faktorî ye, û baştir têgihiştina mekanîzmayên ku di bin danûstendinên di navbera şêwaza jiyanê, hawîrdor û genetîkê de ne, ji bo pêşxistina stratejiyên bi bandor ji bo pêşîgirtin û dermankirinê girîng e [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) Guhertinên Epigenetîk ên Di Zarokan de Bi Xwarina Dayikê re Di Di Ducaniyê de
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.
Veguheztina stabîl a agahdariya epigenetîk di nav gelek nifşan de di pergalên nebat û C de baş tê vegotin. 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.
Digel ku gelek lêkolînan di modelên heywanan de guherînên epîgenetîk ên girêdayî parêzê bi karanîna deverên berendam-malpera-taybet bikar tînin nas kirin, çend analîzên li seranserê genomê hatine kirin. Lêkolînek vê dawîyê balê dikişîne ser destnîşankirina bandora epigenetîk a rasterast a parêzên rûn-rûn / qelewbûna ji ber parêzê di mêşên mezin de ku bi karanîna îfadeya genê ya berfireh a genomê û analîzên methylasyona DNA [43]. Vê lêkolînê 232 herêmên cuda yên methylated (DMRs) di adipocytes de ji mêşên kontrol û bi rûn ên zêde têne xwarin nas kirin. Ya girîng, deverên mirovî yên têkildar ên ji bo DMR-yên mûşê jî di tevna rûnê de ji nifûsa mirovên qelew û bêhêz bi rengekî cihêreng hatin methylated kirin, bi vî rengî parastina pêşveçûna berbiçav a van herêman ronî dike. Ev encam girîngiya muhtemel a DMR-yên naskirî di birêkûpêkkirina homeostaza enerjiyê de di mammalan de tekez dike.
(i) Lêkolînên komeleya genetîkî. 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].
Ji van lêkolînan, metilasyona guhêrbar a PGC1A, HIF3A, ABCG1, û CPT1A û RXRA-ya ku berê hatî destnîşan kirin [18] wekî biyomarkerên ku bi tenduristiya metabolîk ve girêdayî ne, an jî dibe ku pêşbîniya wê, derketin holê ku di heman demê de berendamên maqûl in ji bo rola di pêşkeftina nexweşiya metabolîk de. .
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.
Jîngeha berî zayînê: 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.
Jîngeha piştî zayînê: 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].
Guhertinên metilasyona DNA yên ku bi qelewbûnê ve girêdayî ne an ji hêla parêz an destwerdanên şêwaza jiyanê ve têne çêkirin û kêmbûna giraniyê bi gelemperî nerm in (<15 %), her çend ev li gorî fenotîp û tevna ku hatî lêkolîn kirin diguhere. Mînakî, guhertinên ji %20 mezintir di tevna rûnê de piştî windakirina giraniyê hatine ragihandin [64] û têkiliyên di navbera metilasyona HIF3A û BMI de di tevna rûnê de ji xwînê bêtir diyar bûne [52].
encamên
