Beslenme ve Epigenetik

Year 2018, , 12 - 18, 18.12.2018

Belgin Sırıken , Fatih Sırıken Cengiz Ünsal Gülay Çiftci

https://doi.org/10.31196/huvfd.501391

Cited By: 2

Abstract

Epigenetik, DNA diziliminde herhangi bir değişiklik
olmaksızın kromatin ve DNA’da reverzibil nitelikte meydana gelen moleküler
değişiklikleri kapsayan kalıtsal mitotik çalışmalar olarak tanımlanır. Başlıca epigenetik
süreçler metilasyon, kromatin modifikasyonu, fosforilasyon, ubiquitinilasyon ve
sumuilasyondur. Bunlar arasında, DNA metilasyonu ile kromatin modifikasyonu en
iyi bilinenidir. Kromatin, çekirdekte bir araya getirilen bir protein (histon)
ve DNA kompleksidir. Bu kompleks, mikroRNA’lar ve küçük RNA interferansı (RNA
girişimi) gibi bazı RNA formları, enzimler ve asetil gruplar gibi maddeler
tarafından değiştirilebilir. Bu değişiklikler gen ifadesinin etkilenmesine neden
olarak kromatin yapılarını da değiştirir. Epigenetik modifikasyonlar, büyümenin
kritik dönemlerindeki beslenme ve hastalıklara yol açabilen gen ifadelerindeki
değişmeler arasında potansiyel bir bağlantı sağlar. Bu nedenle, epigenetik
işaretlerin çevre, beslenme ve hastalıklar arasında mekanik bir bağlantı
sağladığı kabul edilmektedir. Besinler ve biyoaktif gıda bileşenleri ya direk
olarak DNA metilasyonu ile histon modifikasyonunu katalize eden enzimleri
inhibe ederek ya da bütün enzimatik reaksiyonlar için gerekli ulaşılabilir
substratları değiştirmek suretiyle epigenetik fenomenleri etkileyebilir. Örneğin,
yeşil çay yapraklarında bulunan folatlar, kahve, hububat taneleri, erik ve kivi
meyvelerinde bulunan sinnamik asit, yeşil çaydan elde edilen
epigallocatechin-3-gallate (EGCG) gibi fenoller, kırmızı üzüm ve ürünlerinde
bulunan resveratrol, turpgillerde bulunan izotiyosiyanat ve sulforafan, keten tohumundaki
lignanlar, selenyum ve bazı vitaminler epigenetik besinler olarak
değerlendirilir. Bu derlemenin amacı epigenetik değişikliklerle
beslenme arasındaki ilişkiyi ortaya koymaktadır.

Keywords

Epigenetik, Besinler, Beslenme, Hastalık

Nutrition and Epigenetic

Abstract

Epigenetics is defined as the
mitotically heritable studies on potentially reversible, molecular
modifications of DNA and chromatin without any alteration in DNA sequence. Many types of epigenetic processes have been identified such as methylation,
chromatin modification, acetylation, phosphorylation, ubiquitylation and
sumolyation. However, DNA methylation and chromatin modification are the best
known epigenetic processes. Chromatin is the a complex of proteins and DNA (histones)
in the nucleus. The complex can be modified by substances such as acetyl
groups, enzymes and some RNA forms like microRNAs and small interfering RNAs.
This modification alters chromatin structure to influence gene expression. Epigenetic modifications provide a potential link
between the nutrition during critical periods in development and changes in
gene expression that may cause disease. It is recognized that epigenetic marks
provide a mechanistic link among environment, nutrition and disease. Nutrients
and bioactive food components can ifluence epigenetic phenomena either directly
by inhibiting enzymes that catalyze DNA metylation, histone modifications, or
by altering the necessary substrates availability for enzymatic reactions. For
example, folate from green leafy vegetables, cinnamic acids from coffee, grain
cereals, plums and kiwifruit, polyphenols like epigallocatechin-3-gallate (EGCG),
resveratrol, sulforaphane and isothiocyanates, lignans from green tea, red
grapes and their products, cruciferous vegetables, linseed, respectively, selenium
and vitamin are considered as epigenetic nutritions. The aim of the review have
shown that the link between nutrition in epigenetic changes.

Keywords

Epigenetic, Nutrition, Diet, Diseases

References

• Altshuler-Keylin S, Kajimura S, 2017: Mitochondrial homeostasis in adipose tissue remodeling. Sci Signal, 10, pii: eaai9248
• Barker DJ, 2004: Developmental origins of adult health and disease. J Epidemiol Community Health, 58 (2), 114-115.
• Barres R, Zierath JR, 2016: The role of diet and exercise in the transgenerational epigenetic landscape of T2DM. Nat Rev Endocrinol, 12, 441-51.
• Bishop KS, Ferguson LR, 2015: The interaction between epigenetics, nutrition and the development of cancer. Nutrients, 7, 922-947.
• Burns CM, Chu H, Rueter SM, Hutchinson LK, Canton H, Sanders-Bush E, Emeson RB, 1997: Regulation of serotonin-2C receptor G-protein coupling by RNA editing. Nature, 387(6630), 303-8.
• Cheng Z, Almeida FA, 2014: Mitochondrial alteration in type 2 diabetes and obesity: an epigenetic link. Cell Cycle,13,890-7.
• Cheng Z, Zheng L, Almeida F, 2018: Epigenetic reprogramming in metabolic disorers: nutritional factors and beyond. JNB, 54,1-10.
• Corona M, Estrada E, Zurita M, 2010: Differential expression of mitochondrial genes between queens and workers during caste determination in the honeybee Apis mellifera. J Exp Biol, 8(11), e1000506.
• Dayeh T, Volkov P, Salo S, Hall E, Nilsson E, Olsson AH, Kirkpatrick CL, Wollheim CB, Eliasson L, Rönn T, Bacos K, Ling C, 2014: Genome-wide DNA methylation analysis of human pancreatic islets from type 2 diabetic and nondiabetic donors identifies candidate genes that influence insulin secretion. PLoS Genet, 10(3) ,e1004160.
• Dolinoy DC, Weidman JR, Jirtle RL, 2007: Epigenetic gene regulation: Linking early developmental environment to adult disease. Reprod Toxicol, 23, 297-307.
• van Dijk SJ, Molloy PL, Varinli H, Morrison JL, Muhlhausler BS, 2015: Epigenetics and human obesity. Int J Obes, 39, 85–97.
• Eser BE, Yazgan ÜC, Gürses AA, Aydın M, 2016. Diabetes Mellitus ve Epigenetik Mekanizmalar. Dicle Tıp Derg, 43 (2), 375-382.
• Fu Y, Dominissini D, Rechavi G, He C, 2014: Gene expression regulation mediated through reversible m(6)A RNA methylation. Nat Rev Genet, 15, 293-306.
• Gluckman PD, Lillycrop KA, Vickers MH, Pleasants AB, Phillips ES, Beedle AS, Burdge GC, Hanson MA, 2007: Metabolic plasticity during mammalian development is directionally dependent on early nutritional status. Proc Natl Acad Sci USA, 104(31), 12796-12800.
• Godfrey KM, Barker DJ, 2001: Fetal programming and adult health. Public Health Nutr, 4, 611-624.
• Gua F, Jen KI, 1995. High feding durng pregnancy and lactation affects offspring metabolism in rats. Physiol Behav, 571, 681-686.
• Hjort L, Jorgensen SW, Gillberg L, Hall E, Brons C, Frystyk J, Vaag AA, Ling C, 2017: 36 h fasting of young men influences adipose tissue DNA methylation of LEP and ADIPOQ in a birth weight-dependent manner. Clin Epigenetics, 9, 40.
• Lawrence M, Daujat S, Schneider R, 2016: Lateral thinking: how histone modifications regulate gene expression. Trends Genet, 32, 42-56.
• Leung A, Parks BW, Du J, Trac C, Setten R, Chen Y, Brown K, Lusis AJ, Natarajan R, Schones DE, 2014: Open chromatin profiling in mice livers reveals unique chromatin variations induced by high fat diet. J Biol Chem, 289, 23557-67.
• Lillycrop KA, Burdge GC, 2012: Epigenetic mechanisms linking early nutrition to long term health. Best Pract Res Clin Endocr Metab, 26, 667-676.
• Liu L, Zheng LD, Donnelly SR, Emont MP, Wu J, Cheng Z, 2017: Isolation of mouse stromal vascular cells for monolayer culture. Methods Mol Biol, 1566, 9-16.
• Merlotti C, Morabito A, Pontiroli AE, 2014: Prevention of type 2 diabetes; a systematic review and meta-analysis of different intervention strategies. Diabetes Obes Metab, 16, 719-27.
• Mudaliar U, Zabetian A, Goodman M, Echouffo-Tcheugui JB, Albright AL, Gregg EW, Mohammed KA, 2016: Cardiometabolic risk factor changes observed in diabetes prevention programs in US settings: a systematic review and meta-analysis. PLoS Med, 13, e1002095.
• Ng SF, Lin RC, Laybutt DR, Barres R, Owens JA, Morris MJ, 2010: Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring. Nature, 467, 963-966.
• Nilsson E, Jansson PA, Perfilyev A, Volkov P, Pedersen M, Svensson MK, Poulsen P, Ribel-Madsen R, Pedersen NL, Almgren P, Fadsta J, Rönn T, Klarlund Pedersen B, Scheele C, Vaag A, Ling C, 2014: Altered DNA methylation and differential expression of genes influencing metabolism and inflammation in adipose tissue from subjects with type 2 diabetes. Diabetes, 63, 2962-76.
• Rutkowski JM, Stern JH, Scherer PE, 2015: The cell biology of fat expansion. J Cell Biol, 208,501-12.
• Supic G, Jagodic M, Magic Z, 2013: Epigenetics: A New Link Between Nutrition and Cancer. Nutr Cancer, 65, 781-792.
• Torrens C, Brawley L, Dance CS, Itoh S, Poston L, Hanson MA, 2002: First evidence for transgenerational vascular programming in the rat protein restriction model. J Physiol, 543, 41-42.
• Jacobsen SC, Gillberg L, Bork-Jensen J, Ribel-Madsen R, Lara E, Calvanese V, Ling C, Fernandez AF, Fraga MF, Poulsen P, Brøns C, Vaag A, 2014: Young men with low birthweight exhibit decreased plasticity of genome-wide muscle DNA methylation by high-fat overfeeding. Diabetologia, 57,1154-8.
• Karlsson O, Baccarelli AA, 2016: Environmental health and long non-coding RNAs. Curr Environ Health Rep, 3,178-87.
• Khare S, Verma M, 2012:Epigenetics of colon cancer. Methods Mol Biol, 863, 177-185.
• Klose JR, Bird AP, 2006: Genomic DNA methylation: the mark and its mediators. Trends Biochem Sci, 31(2), 90-97.
• Langley-Evana SC, Sculley DV, 2005: Programming of hepatic antioxidant capacity and oxidative injury in the ageing rat. Mech Ageing Dev, 126 (6-7), 804-812.
• Leung A, Parks BW, Du J, Trac C, Setten R, Chen Y, Brown K, Lusis AJ, Natarajan R, Schones DE, 2014: Open chromatin profiling in mice livers reveals unique chromatin variations induced by high fat diet. J Biol Chem, 289, 23557-67.
• Liu L, Zheng LD, Donnelly SR, Emont MP, Wu J, Cheng Z, 2017: Isolation of mouse stromal vascular cells for monolayer culture. Methods Mol Biol, 1566, 9-16.
• Locke AE, Kahali B, Berndt SI, Justice AE, Pers TH, Day FR, et al., 2015: Genetic studies of body mass index yield new insights for obesity biology. Nature, 518, 197-206.
• Painter RC, Roseboom TJ, Bleker OP, 2005: Prenatal exposure to the Dutch famine and disease in later life: an overview. Repro Toxicol, 20, 345-352.
• Portela A, Esteller M, 2010: Epigenetic modification and human disease. Nat Biotechnol, 28(10), 1057-1068.
• Pietilainen KH, Ismail K, Jarvinen E, Heinonen S, Tummers M, Bollepalli S, Lyle R, Muniandy M, Moilanen E, Hakkarainen A, Lundbom J, Lundbom N, Rissanen A, Kaprio J, Ollikainen M, 2016: DNA methylation and gene expression patterns in adipose tissue differ significantly within young adult monozygotic BMI-discordant twin pairs. Int J Obes,40, 654-61.
• Schwenk RW, Vogel H, Schurmann A, 2013: Genetic and epigenetic control of metabolic health. Mol Metab, 2, 337-47.
• Schones DE, Leung A, Natarajan R, 2015: Chromatin modifications associated with diabetes and obesity. ATVB, 35, 1557-61.
• Waddington C, 1940: Organisers and genes. UK Cambridge University Press, Cambridge.
• Youngson NA, 2008: Whitelaw, E. Transgenerational epigenetic effects. Annu Rev Genom Hum G, 9, 233-257.