Academic literature on the topic 'Dietary methyl donors'

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Journal articles on the topic "Dietary methyl donors"

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Cronje, P. B. "Essential role of methyl donors in animal productivity." Animal Production Science 58, no. 4 (2018): 655. http://dx.doi.org/10.1071/an15729.

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Dietary requirements for the methyl donors, choline, betaine and folate, in livestock species are poorly defined and have not been included in diet formulation software or simulation models for animals. A deficiency of methyl donors may promote an inflammatory state, which is significant for the livestock industry because chronic low-grade inflammation is widespread among livestock under commercial conditions. Furthermore, recent evidence showing that methyl donors activate adenosine monophosphate-activated protein kinase, an anti-inflammatory master switch, indicates that dietary methyl-donor
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Batra, Vipen, Vellappan Kesavan та Kaushala P. Mishra. "Modulation of DNA Methyltransferase 1 Profile by γ-lrradiation Followed by Methyl Donor Starvation". Pteridines 16, № 4 (2005): 159–65. http://dx.doi.org/10.1515/pteridines.2005.16.4.159.

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Abstract Role of one-carbon transfer agents methyl donors namely folate, choline and methionine in DNA methylation has been the subject of extensive investigation. The methylation pattern of DNA is established during embryogenesis and is subsequently maintained by maintenance methylation activity of the enzyme DNA methyltransferase 1 (dnmt 1). Ionizing radiation is known to extensively damage the DNA. Folate, a water-soluble vitamin, is known to contribute towards repair of damaged DNA due to its role in synthesis of nucleotide base adenine, guanine and thymidylate. Sufficient dietary availabi
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Batistel, Fernanda. "145 Nutritional Advances in Fetal and Neonatal Development: Methyl Donors." Journal of Animal Science 98, Supplement_3 (2020): 122–23. http://dx.doi.org/10.1093/jas/skaa054.209.

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Abstract The objective of this presentation is to discuss and review research on methyl donors in the developmental programming of dairy cattle. One-carbon metabolism is catalyzed by several enzymes in the presence of dietary micronutrients, including methionine, choline, betaine, and folate, and generates S-adenosylmethionine. S-adenosylmethionine is crucial for numerous cellular functions such as DNA and histone methylation as well as protein synthesis. Despite the biological role of S-adenosylmethionine, there is a limited understanding of the impact of dietary methyl donors’ supply to preg
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Kiss, Eva, Gertrud Forika, Reka Mohacsi, Zsuzsanna Nemeth, Tibor Krenacs, and Magdolna Dank. "Methyl-Donors Can Induce Apoptosis and Attenuate Both the Akt and the Erk1/2 Mediated Proliferation Pathways in Breast and Lung Cancer Cell Lines." International Journal of Molecular Sciences 22, no. 7 (2021): 3598. http://dx.doi.org/10.3390/ijms22073598.

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Dietary methyl-donors play important roles in physiological processes catalyzed by B vitamins as coenzymes, and are used for complementary support in oncotherapy. Our hypothesis was that methyl-donors can not only assist in tolerating cancer treatment but may also directly interfere with tumor growth and proliferation. Therefore, we investigated the proposed cancer inhibitory effects of methyl-donors (in a mixture of L-methionine, choline chloride, folic acid, and vitamin B12) on MCF7 and T47D breast cancer as well as A549 and H1650 lung cancer cell lines. Indeed, methyl-donor treatment signif
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Robinson, Jason Lorne. "The effects of dietary methyl donors on methionine partitioning in the neonatal piglet." Applied Physiology, Nutrition, and Metabolism 40, no. 11 (2015): 1218. http://dx.doi.org/10.1139/apnm-2015-0362.

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The metabolism of the indispensable amino acid methionine is critical during development. Methionine is used to synthesize protein for growth and, using the methionine cycle, it is the precursor of >50 critical nutrients and contributes to epigenetic regulation. Therefore, the dietary methionine requirement must factor all the potential roles of methioine. Three major processes summarize the methionine cycle: transmethylation (TM), which transfers methyl groups to nutrient precursors and DNA; transsulfuration (TS), which represents methionine disposal; and remethylation (RM), which resynthe
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Shabbeer, Shabana, Simon A. Williams, Brian W. Simons, James G. Herman, and Michael A. Carducci. "Progression of Prostate Carcinogenesis and Dietary Methyl Donors: Temporal Dependence." Cancer Prevention Research 5, no. 2 (2011): 229–39. http://dx.doi.org/10.1158/1940-6207.capr-11-0357.

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Pinotti, L., A. Baldi, and V. Dell'Orto. "Comparative mammalian choline metabolism with emphasis on the high-yielding dairy cow." Nutrition Research Reviews 15, no. 2 (2002): 315–32. http://dx.doi.org/10.1079/nrr200247.

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AbstractThe present review examines the importance of choline in dairy cow nutrition. Choline is an essential nutrient for mammals when excess methionine and folate are not available in the diet. The requirement for choline can be met by dietary choline and by transmethylation reactions. Two types of functions for choline are known: functions of choline per se; functions as a methyl donor. The two principal methyl donors in animal metabolism are betaine, a metabolite of choline, and S-adenosyl-methionine, a metabolite of methionine. Choline and methionine are interchangeable with regard to the
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Wooldridge, Amy L., Robert J. Bischof, Hong Liu, et al. "Late-gestation maternal dietary methyl donor and cofactor supplementation in sheep partially reverses protection against allergic sensitization by IUGR." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 1 (2018): R22—R33. http://dx.doi.org/10.1152/ajpregu.00549.2016.

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Perinatal exposures are associated with altered risks of childhood allergy. Human studies and our previous work suggest that restricted growth in utero (IUGR) is protective against allergic disease. The mechanisms are not clearly defined, but reduced fetal abundance and altered metabolism of methyl donors are hypothesized as possible underlying mechanisms. Therefore, we examined whether late-gestation maternal dietary methyl donor and cofactor supplementation of the placentally restricted (PR) sheep pregnancy would reverse allergic protection in progeny. Allergic outcomes were compared between
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Cordero, P., F. I. Milagro, J. Campion, and J. A. Martinez. "Supplementation with methyl donors during lactation to high-fat-sucrose-fed dams protects offspring against liver fat accumulation when consuming an obesogenic diet." Journal of Developmental Origins of Health and Disease 5, no. 5 (2014): 385–95. http://dx.doi.org/10.1017/s204017441400035x.

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Methyl donor supplementation has been reported to prevent obesity-induced liver fat accumulation in adult rats. We hypothesized that this protection could be mediated by perinatal nutrition. For this purpose, we assessed the response to an obesogenic diet (high-fat-sucrose, HFS) during adulthood depending on maternal diet during lactation. Female Wistar rats fed control diet during pregnancy were assigned to four postpartum dietary groups: control, control supplemented with methyl donors (choline, betaine, folic acid, vitamin B12), HFS and HFS supplemented with methyl donors. At weaning, the m
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Newberne, Paul M., Voranunt Suphiphat, Mary Locniskar, and Joao L. V. de Camargo. "Inhibition of hepatocarcinogenesis in mice by dietary methyl donors methionine and choline." Nutrition and Cancer 14, no. 3-4 (1990): 175–81. http://dx.doi.org/10.1080/01635589009514092.

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Dissertations / Theses on the topic "Dietary methyl donors"

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McGee, Meghan. "The Association Between Dietary Methyl Donor Intake During Pregnancy and Offspring Birth Weight." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34582.

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Maternal consumption of dietary methyl donors (DMDs) such as folate, methionine, choline, as well as co-factors including zinc, vitamins B2, B6 and B12 can lead to permanent alterations in the DNA and gene expression of the developing fetus. This study aimed to identify patterns of DMD intake during the second trimester of pregnancy and their associations with infant birth weight, small and large for gestational age (SGA and LGA, respectively). From food sources alone, most pregnant women were below the estimated average requirement for dietary folate equivalent (DFE) (69%) and below the adequ
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Dürr, Julia. "Folate, choline, betaine, resistant starch & dietary fiber in Swedish lentils : Effect of cultivar and growing conditions." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-96847.

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Background: One key component in the development of sustainable farming and foodstuffs is to increase the cultivation of legumes, due to their environmental and health benefits. Legumes contain several essential vitamins and minerals, protein and fiber, but cultivation can be problematic due to their weak stem strength which results in loss of crops as a result of crop lodging and susceptibility to weed invasion. One possible solution is co-cultivation with cereal crops such as oats as they provide support and outcompete weed growth, however, it is still unknown if co-cultivation will affect t
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Konycheva, Galina. "Effects of prenatal dietary methyl donor deficiency on development and epigenetic mechanisms in offspring : studies in the rat." Thesis, University of Auckland, 2010. http://hdl.handle.net/2292/5635.

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Human epidemiological and animal studies suggest that unbalanced maternal diet during pregnancy leads to low birth weight and predisposes offspring to the development of a number of pathological conditions like metabolic and cardiovascular diseases. This effect is referred to as fetal or developmental programming, however the underlying mechanism is yet unknown. An epigenetic mechanism of gene regulation, DNA methylation, has been suggested as a strong candidate for the underling mechanism of developmental programming due to the fact that establishment of DNA methylation patterns begins
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Book chapters on the topic "Dietary methyl donors"

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de Conti, Aline, and Igor P. Pogribny. "Epigenetics of Dietary Methyl-Group Donor Deficiency and Liver Cancer." In Handbook of Nutrition, Diet, and Epigenetics. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55530-0_43.

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de Conti, Aline, and Igor P. Pogribny. "Epigenetics of Dietary Methyl-Group Donor Deficiency and Liver Cancer." In Handbook of Nutrition, Diet, and Epigenetics. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-31143-2_43-1.

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Sanblas, Mirian, Xabier Bengoetxea, Fermin Milagro, and Maria J. Ramirez. "Linking dietary methyl donors, maternal separation, and depression." In The Neuroscience of Depression. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-817935-2.00046-5.

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Eryılmaz Pehlivan, Fadime. "Diet-Epigenome Interactions: Epi-Drugs Modulating the Epigenetic Machinery During Cancer Prevention." In Epigenetics - “A Parallel Universe” in the Study of Cancer Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95374.

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The roles of diet and environment on health have been known since ancient times. Cancer is both a genetic and an epigenetic disease and a complex interplay mechanism of genetic and environmental factors composed of multiple stages in which gene expression, protein and metabolite function operate synchronically. Disruption of epigenetic processes results in life-threatening diseases, in particular, cancer. Epigenetics involves altered gene expression without any change of nucleotide sequences, such as DNA methylation, histone modifications and non-coding RNAs in the regulation of genome. According to current studies, cancer is preventable with appropriate or balanced food and nutrition, in some cases. Nutrient intake is an environmental factor, and dietary components play an importent role in both cancer development and prevention. Due to epigenetic events induce changes in DNA and thus influencing over all gene expression in response to the food components, bioactive compounds and phytochemicals as potent antioxidants and cancer preventive agents have important roles in human diet. Several dietray components can alter cancer cell behavior and cancer risk by influencing key pathways and steps in carcinogenesis, including signaling, apoptosis, differentiation, or inflammation. To date, multiple biologically active food components are strongly suggested to have protective potential against cancer formation, such as methyl-group donors, fatty acids, phytochemicals, flavonoids, isothiocyanates, etc. Diet considered as a source of either carcinogens that are present in certain foods or acting in a protective manner such as vitamins, antioxidants, detoxifying substances, chelating agents etc. Thus, dietary phytochemicals as epigenetic modifiers in cancer and effects of dietary phytochemicals on gene expression and signaling pathways have been widely studied in cancer. In this chapter, current knowledge on interactions between cancer metabolism, epigenetic gene regulation, and how both processes are affected by dietary components are summerized. A comprehensive overview of natural compounds with epigenetic activity on tumorogenesis mechanisms by which natural compounds alter the cancer epigenome is provided. Studies made in epigenetics and cancer research demonstrated that genetic and epigenetic mechanisms are not separate events in cancer; they influence each other during carcinogenesis, highlighting plant-derived anticancer compounds with epigenetic mechanisms of action, and potential use in epigenetic therapy. Recent investigations involving epigenetic modulations suggest that diet rich in phytochemicals not only reduce the risk of developing cancer, but also affect the treatment outcome.
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Conference papers on the topic "Dietary methyl donors"

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Hanley, Matthew P., and Daniel W. Rosenberg. "Abstract 899: Cancer protection associated with dietary methyl donor deficiency is characterized by persistent changes to epithelial proliferation and metabolism." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-899.

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