scholarly journals Parental Selenium Nutrition Affects the One-Carbon Metabolism and the Hepatic DNA Methylation Pattern of Rainbow Trout (Oncorhynchus mykiss) in the Progeny

Life ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 121 ◽  
Author(s):  
Pauline Wischhusen ◽  
Takaya Saito ◽  
Cécile Heraud ◽  
Sadasivam J. Kaushik ◽  
Benoit Fauconneau ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Rainbow Trout ◽  
Carbon Metabolism ◽  
Methylation Pattern ◽  
Mrna Levels ◽  
Transsulfuration Pathway ◽  
Methionine Cycle ◽  
Dna Methylation Pattern ◽  
One Carbon Metabolism ◽  
The One

Selenium is an essential micronutrient and its metabolism is closely linked to the methionine cycle and transsulfuration pathway. The present study evaluated the effect of two different selenium supplements in the diet of rainbow trout (Onchorhynchus mykiss) broodstock on the one-carbon metabolism and the hepatic DNA methylation pattern in the progeny. Offspring of three parental groups of rainbow trout, fed either a control diet (NC, basal Se level: 0.3 mg/kg) or a diet supplemented with sodium selenite (SS, 0.8 mg Se/kg) or hydroxy-selenomethionine (SO, 0.7 mg Se/kg), were collected at swim-up fry stage. Our findings suggest that parental selenium nutrition impacted the methionine cycle with lower free methionine and S-adenosylmethionine (SAM) and higher methionine synthase (mtr) mRNA levels in both selenium-supplemented treatments. DNA methylation profiling by reduced representation bisulfite sequencing (RRBS) identified differentially methylated cytosines (DMCs) in offspring livers. These DMCs were related to 6535 differentially methylated genes in SS:NC, 6890 in SO:NC and 7428 in SO:SS, respectively. Genes with the highest methylation difference relate, among others, to the neuronal or signal transmitting and immune system which represent potential targets for future studies.

Long-term effect of parental selenium supplementation on the one-carbon metabolism in rainbow trout (Oncorhynchus mykiss) fry exposed to hypoxic stress

2021 ◽  
pp. 1-12
Author(s):  
Pauline Wischhusen ◽  
Cécile Heraud ◽  
Kaja Skjærven ◽  
Sadasivam J. Kaushik ◽  
Benoit Fauconneau ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Carbon Metabolism ◽  
Control Diet ◽  
Whole Body ◽  
Mrna Levels ◽  
Hypoxic Stress ◽  
Adenosylmethionine Decarboxylase ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
One Carbon Metabolism ◽  
The One

Abstract This study evaluated how different forms of selenium (Se) supplementation into rainbow trout broodstock diets modified the one-carbon metabolism of the progeny after the beginning of exogenous feeding and followed by hypoxia challenge. The progeny of three groups of rainbow trout broodstock fed either a control diet (Se level: 0·3 µg/g) or a diet supplemented with inorganic sodium selenite (Se level: 0·6 µg/g) or organic hydroxy-selenomethionine (Se level: 0·6 µg/g) was cross-fed with diets of similar Se composition for 11 weeks. Offspring were sampled either before or after being subjected to an acute hypoxic stress (1·7 mg/l dissolved oxygen) for 30 min. In normoxic fry, parental Se supplementation allowed higher glutathione levels compared with fry originating from parents fed the control diet. Parental hydroxy-selenomethionine treatment also increased cysteine and cysteinyl–glycine concentrations in fry. Dietary Se supplementation decreased glutamate–cysteine ligase (cgl) mRNA levels. Hydroxy-selenomethionine feeding also lowered the levels of some essential free amino acids in muscle tissue. Supplementation of organic Se to parents and fry reduced betaine-homocysteine S-methyltransferase (bhmt) expression in fry. The hypoxic stress decreased whole-body homocysteine, cysteine, cysteinyl-glycine and glutathione levels. Together with the higher mRNA levels of cystathionine beta-synthase (cbs), a transsulphuration enzyme, this suggests that under hypoxia, glutathione synthesis through transsulphuration might have been impaired by depletion of a glutathione precursor. In stressed fry, S-adenosylmethionine levels were significantly decreased, but S-adenosylhomocysteine remained stable. Decreased bhmt and adenosylmethionine decarboxylase 1a (amd1a) mRNA levels in stressed fry suggest a nutritional programming by parental Se also on methionine metabolism of rainbow trout.

scholarly journals Germline polymorphisms in the one-carbon metabolism pathway and DNA methylation in colorectal cancer

2009 ◽  
Vol 21 (3) ◽  
pp. 331-345 ◽  
Author(s):  
Aditi Hazra ◽  
Charles S. Fuchs ◽  
Takako Kawasaki ◽  
Gregory J. Kirkner ◽  
David J. Hunter ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Carbon Metabolism ◽  
Metabolism Pathway ◽  
One Carbon Metabolism ◽  
The One

scholarly journals Abnormal Homocysteine Metabolism: An Insight of Alzheimer’s Disease from DNA Methylation

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Tingting Pi ◽  
Bo Liu ◽  
Jingshan Shi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Carbon Metabolism ◽  
The Elderly ◽  
Epigenetic Mechanisms ◽  
Related Substance ◽  
The Central Nervous System ◽  
One Carbon Metabolism ◽  
The One

Alzheimer’s disease (AD) is a chronic neurodegenerative disease in the central nervous system that has complex pathogenesis in the elderly. The current review focuses on the epigenetic mechanisms of AD, according to the latest findings. One of the best-characterized chromatin modifications in epigenetic mechanisms is DNA methylation. Highly replicable data shows that AD occurrence is often accompanied by methylation level changes of the AD-related gene. Homocysteine (Hcy) is not only an intermediate product of one-carbon metabolism but also an important independent risk factor of AD; it can affect the cognitive function of the brain by changing the one-carbon metabolism and interfering with the DNA methylation process, resulting in cerebrovascular disease. In general, Hcy may be an environmental factor that affects AD via the DNA methylation pathway with a series of changes in AD-related substance. This review will concentrate on the relation between DNA methylation and Hcy and try to figure out their rule in the pathophysiology of AD.

scholarly journals Maternal High-Fat Diet Disrupted the One-Carbon Metabolic Process and Epigenetic Regulation in Offspring Male Mice for Non-Alcoholic Fatty Liver Disease (P11-142-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Hui Peng ◽  
Jiangyuan Li ◽  
Zhimin Liu ◽  
Ernest Lynch ◽  
Zehuan Ding ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Carbon Metabolism ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Dna Hypermethylation ◽  
Alcoholic Fatty Liver ◽  
Methionine Cycle ◽  
One Carbon Metabolism ◽  
The One ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives Pregnant women may transmit their metabolic phenotype to offspring, enhancing the risk for non-alcoholic fatty liver disease (NAFLD) in the next generation; however, the molecular mechanisms remain unclear. In the present study, we hypothesized that the maternal HF diet disrupts one-carbon metabolism with a consequent methylation change in the offspring liver that contributes to a worsen NAFLD induced by postweaning high-fat (HF) diet. Methods To test our hypothesis, we used offspring mice exposed to either maternal HF diet (HF group), or an early transition to a maternal NF diet before pregnancy (H9N group), or maternal methyl donor supplement (H1S or H2S group), comparing to the offspring with normal-fat diet (NF group). Results The HF offspring displayed obesity, glucose intolerance and hepatic steatosis, the H9N offspring avoided all, while the H1S and H2S offspring released hepatic steatosis only. Data from the gene expression study suggested a disruption of pathways involved in the one-carbon metabolism in the HF offspring with a restoration in the H9N, the H1S and the H2S offspring. Furthermore, we showed a disruption of methionine cycle associated with DNA hypermethylation and a de-production of L-carnitine and PPAR-α in the HF, but not the H9N offspring. However, the H1S and H2S diet only normalized the methionine cycle and restored L-carnitine and PPAR-α content, but not rescued the DNA hypermethylation in offspring liver. Thus, we proved that the maternal HF diet disrupted the methionine cycle and further led to methylation changes for mitochondrial dysfunction and fatty acid oxidation responsible for the fatty liver, rather than for the global DNA hypermethylation, which might contribute to the obesity and glucose intolerance. Conclusions Our study provides a novel mechanism to understand the lipid metabolism and epigenetics in transgeneration. More importantly, it suggested to us a potentially effective diet intervention strategy to reduce the transgeneration risk for NAFLD. Funding Sources This project is supported by grants from the National Institutes of Health. This work is supported by the USDA National Institute of Food and Agriculture.

scholarly journals Unique adaptations in neonatal hepatic transcriptome, nutrient signaling, and one-carbon metabolism in response to feeding ethyl cellulose rumen-protected methionine during late-gestation in Holstein cows

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Valentino Palombo ◽  
Abdulrahman Alharthi ◽  
Fernanda Batistel ◽  
Claudia Parys ◽  
Jessie Guyader ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Immune Responses ◽  
Carbon Metabolism ◽  
Ethyl Cellulose ◽  
In Utero ◽  
Holstein Cows ◽  
Nutrient Metabolism ◽  
Transsulfuration Pathway ◽  
One Carbon Metabolism ◽  
Hepatic Transcriptome

Abstract Background Methionine (Met) supply during late-pregnancy enhances fetal development in utero and leads to greater rates of growth during the neonatal period. Due to its central role in coordinating nutrient and one-carbon metabolism along with immune responses of the newborn, the liver could be a key target of the programming effects induced by dietary methyl donors such as Met. To address this hypothesis, liver biopsies from 4-day old calves (n = 6/group) born to Holstein cows fed a control or the control plus ethyl-cellulose rumen-protected Met for the last 28 days prepartum were used for DNA methylation, transcriptome, metabolome, proteome, and one-carbon metabolism enzyme activities. Results Although greater withers and hip height at birth in Met calves indicated better development in utero, there were no differences in plasma systemic physiological indicators. RNA-seq along with bioinformatics and transcription factor regulator analyses revealed broad alterations in ‘Glucose metabolism’, ‘Lipid metabolism, ‘Glutathione’, and ‘Immune System’ metabolism due to enhanced maternal Met supply. Greater insulin sensitivity assessed via proteomics, and efficiency of transsulfuration pathway activity suggested beneficial effects on nutrient metabolism and metabolic-related stress. Maternal Met supply contributed to greater phosphatidylcholine synthesis in calf liver, with a role in very low density lipoprotein secretion as a mechanism to balance metabolic fates of fatty acids arising from the diet or adipose-depot lipolysis. Despite a lack of effect on hepatic amino acid (AA) transport, a reduction in metabolism of essential AA within the liver indicated an AA ‘sparing effect’ induced by maternal Met. Conclusions Despite greater global DNA methylation, maternal Met supply resulted in distinct alterations of hepatic transcriptome, proteome, and metabolome profiles after birth. Data underscored an effect on maintenance of calf hepatic Met homeostasis, glutathione, phosphatidylcholine and taurine synthesis along with greater efficiency of nutrient metabolism and immune responses. Transcription regulators such as FOXO1, PPARG, E2F1, and CREB1 appeared central in the coordination of effects induced by maternal Met. Overall, maternal Met supply induced better immunometabolic status of the newborn liver, conferring the calf a physiologic advantage during a period of metabolic stress and suboptimal immunocompetence.

Uteroplacental insufficiency alters DNA methylation, one-carbon metabolism, and histone acetylation in IUGR rats

2004 ◽  
Vol 18 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Nicole K. MacLennan ◽  
S. Jill James ◽  
Stephan Melnyk ◽  
Ali Piroozi ◽  
Stefanie Jernigan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Histone Acetylation ◽  
Carbon Metabolism ◽  
Hepatic Gene Expression ◽  
Mrna Levels ◽  
Dna Hypomethylation ◽  
Artery Ligation ◽  
Transient Nature ◽  
One Carbon Metabolism

Uteroplacental insufficiency leads to intrauterine growth retardation (IUGR) and increases the risk of insulin resistance and hypertriglyceridemia in both humans and rats. Postnatal changes in hepatic gene expression characterize the postnatal IUGR rat, despite the transient nature of the initial in utero insult. Phenomena such as DNA methylation and histone acetylation can induce a relatively static reprogramming of gene transcription by altering chromatin infrastructure. We therefore hypothesized that uteroplacental insufficiency persistently affects DNA methylation and histone acetylation in the IUGR rat liver. IUGR rat pups were created by inducing uteroplacental insufficiency through bilateral uterine artery ligation of the pregnant dam on day 19 of gestation. The SssI methyltransferase assay and two-dimensional thin-layer chromatography demonstrated genome-wide DNA hypomethylation in postnatal IUGR liver. To investigate a possible mechanism for this hypomethylation, levels of hepatic metabolites and enzyme mRNAs involved in one-carbon metabolism were measured using HPLC with coulometric electrochemical detection and real-time RT-PCR, respectively. Uteroplacental insufficiency increased IUGR levels of S-adenosylhomocysteine, homocysteine, and methionine in association with decreased mRNA levels of methionine adenosyltransferase and cystathionine-β-synthase. Western blotting further demonstrated that increased quantities of acetylated histone H3 also characterized the IUGR liver. Increased hepatic levels of S-adenosylhomocysteine can promote DNA hypomethylation, which is often associated with histone hyperacetylation. We speculate that the altered intrauterine milieu associated with uteroplacental insufficiency affects hepatic one-carbon metabolism and subsequent DNA methylation, which thereby alters chromatin dynamics and leads to persistent changes in hepatic gene expression.

scholarly journals Alterations in One-Carbon Metabolism in Celiac Disease

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3723
Author(s):  
Rafael Martín-Masot ◽  
Natàlia Mota-Martorell ◽  
Mariona Jové ◽  
José Maldonado ◽  
Reinald Pamplona ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Carbon Metabolism ◽  
Dietary Treatment ◽  
Transsulfuration Pathway ◽  
Healthy Control ◽  
One Carbon Metabolism ◽  
The One ◽  
Folate Cycle ◽  
First Time ◽  
Metabolomic Study

Celiac disease (CD) is an autoimmune enteropathy associated with alterations of metabolism. Metabolomics studies, although limited, showed changes in choline, choline-derived lipids, and methionine concentrations, which could be ascribed to alterations in one-carbon metabolism. To date, no targeted metabolomics analysis investigating differences in the plasma choline/methionine metabolome of CD subjects are reported. This work is a targeted metabolomic study that analyzes 37 metabolites of the one-carbon metabolism in 17 children with CD, treated with a gluten-free diet and 17 healthy control siblings, in order to establish the potential defects in this metabolic network. Our results demonstrate the persistence of defects in the transsulfuration pathway of CD subjects, despite dietary treatment, while choline metabolism, methionine cycle, and folate cycle seem to be reversed and preserved to healthy levels. These findings describe for the first time, a metabolic defect in one-carbon metabolism which could have profound implications in the physiopathology and treatment of CD.

scholarly journals Formate can differentiate between hyperhomocysteinemia due to impaired remethylation and impaired transsulfuration

2012 ◽  
Vol 302 (1) ◽  
pp. E61-E67 ◽  
Author(s):  
Simon G. Lamarre ◽  
Anne M. Molloy ◽  
Stacey N. Reinke ◽  
Brian D. Sykes ◽  
Margaret E. Brosnan ◽  
...  
Keyword(s):  
Carbon Metabolism ◽  
Folate Metabolism ◽  
Methionine Synthase ◽  
Vitamin B ◽  
Metabolomic Analysis ◽  
Elevated Plasma ◽  
H Nmr ◽  
Transsulfuration Pathway ◽  
One Carbon Metabolism ◽  
The One

Formate can differentiate between hyperhomocysteinemia due to impaired remethylation and impaired transsulfuration. Am J Physiol Endocrinol Metab 301: E000–E000, 2011. First published September 20, 2011; 10.1152/ajpendo.00345.2011.—We carried out a1H-NMR metabolomic analysis of sera from vitamin B12-deficient rats. In addition to the expected increases in methylmalonate and homocysteine (Hcy), we observed an approximately sevenfold increase in formate levels, from 64 μM in control rats to 402 μM in vitamin B12-deficient rats. Urinary formate was also elevated. This elevation of formate could be attributed to impaired one-carbon metabolism since formate is assimilated into the one-carbon pool by incorporation into 10-formyl-THF via the enzyme 10-formyl-THF synthase. Both plasma and urinary formate were also increased in folate-deficient rats. Hcy was elevated in both the vitamin B12- and folate-deficient rats. Although plasma Hcy was also elevated, plasma formate was unaffected in vitamin B6-deficient rats (impaired transsulfuration pathway). These results were in accord with a mathematical model of folate metabolism, which predicted that reduction in methionine synthase activity would cause increased formate levels, whereas reduced cystathionine β-synthase activity would not. Our data indicate that formate provides a novel window into cellular folate metabolism, that elevated formate can be a useful indicator of deranged one-carbon metabolism and can be used to discriminate between the hyperhomocysteinemia caused by defects in the remethylation and transsulfuration pathways.

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