scholarly journals Perinatal high fat diet and early life methyl donor supplementation alter one carbon metabolism and DNA methylation in the brain

2018 ◽  
Vol 145 (5) ◽  
pp. 362-373 ◽  
Author(s):  
Sarah E. McKee ◽  
Sisi Zhang ◽  
Li Chen ◽  
Joshua D. Rabinowitz ◽  
Teresa M. Reyes
Keyword(s):  
Dna Methylation ◽  
Carbon Metabolism ◽  
High Fat Diet ◽  
Early Life ◽  
High Fat ◽  
Methyl Donor ◽  
One Carbon Metabolism ◽  
The Brain

scholarly journals Assessment of DNA Methylation and Oxidative Changes in the Heart and Brain of Rats Receiving a High-Fat Diet Supplemented with Various Forms of Chromium

Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1470
Author(s):  
Wojciech Dworzański ◽  
Ewelina Cholewińska ◽  
Bartosz Fotschki ◽  
Jerzy Juśkiewicz ◽  
Piotr Listos ◽  
...  
Keyword(s):  
Dna Methylation ◽  
High Fat Diet ◽  
Protein Carbonyl ◽  
Global Dna Methylation ◽  
Standard Diet ◽  
Epigenetic Changes ◽  
Oxidation Reactions ◽  
High Fat ◽  
Repair Enzymes ◽  
The Brain

The aim of the study was to determine how feeding rats a high-fat diet supplemented with various forms of chromium affects DNA methylation and oxidation reactions as well as the histology of heart and brain tissue. The rats received standard diet or high-fat diet and chromium at 0.3 mg/kg body weight (BW) in form of chromium (III) picolinate, chromium (III)-methionine, or nano-sized chromium. The content of malondialdehyde (MDA), protein carbonyl (PC), and 8-hydroxydeoxyguanosine (8-OHDG), the level of global DNA methylation and the activity of selected DNA repair enzymes were determined in the blood. In the brain and heart, the content of MDA, PC, 8-OHDG, and levels of global DNA methylation were determined. The brain was subjected to histological examination. The use of a high-fat diet was found to intensify epigenetic changes and oxidation reactions in the heart and brain. It was concluded that epigenetic changes and oxidation of lipids, proteins, and DNA in the heart and brain of rats resulting from the use of a high-fat diet cannot be limited by supplementing the diet with chromium. It was established that the use of chromium to supplement a high-fat diet intensifies the negative epigenetic and oxidative changes in the heart and brain, especially in the case of chromium nanoparticles.

Betaine supplementation prevents fatty liver induced by a high-fat diet: effects on one-carbon metabolism

Amino Acids ◽  
2015 ◽  
Vol 47 (4) ◽  
pp. 839-846 ◽  
Author(s):  
Rafael Deminice ◽  
Robin P. da Silva ◽  
Simon G. Lamarre ◽  
Karen B. Kelly ◽  
René L. Jacobs ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Carbon Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
One Carbon Metabolism ◽  
Betaine Supplementation

scholarly journals Methyl Donor Nutrients in Chronic Kidney Disease: Impact on the Epigenetic Landscape

2019 ◽  
Vol 149 (3) ◽  
pp. 372-380 ◽  
Author(s):  
Denise Mafra ◽  
Marta Esgalhado ◽  
Natalia A Borges ◽  
Ludmila F M F Cardozo ◽  
Milena B Stockler-Pinto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Kidney Disease ◽  
Dna Methylation ◽  
Kidney Disease ◽  
Carbon Metabolism ◽  
Epigenetic Landscape ◽  
Methyl Donor ◽  
Disease Impact ◽  
One Carbon Metabolism ◽  
Altered Gene

ABSTRACT Epigenetic alterations, such as those linked to DNA methylation, may potentially provide molecular explanations for complications associated with altered gene expression in illnesses, such as chronic kidney disease (CKD). Although both DNA hypo- and hypermethylation have been observed in the uremic milieu, this remains only a single aspect of the epigenetic landscape and, thus, of any biochemical dysregulation associated with CKD. Nevertheless, the role of uremia-promoting alterations on the epigenetic landscape regulating gene expression is still a novel and scarcely studied field. Although few studies have actually reported alterations of DNA methylation via methyl donor nutrient intake, emerging evidence indicates that nutritional modification of the microbiome can affect one-carbon metabolism and the capacity to methylate the genome in CKD. In this review, we discuss the nutritional modifications that may affect one-carbon metabolism and the possible impact of methyl donor nutrients on the microbiome, CKD, and its phenotype.

scholarly journals Correction: Hepatic Methionine Homeostasis Is Conserved in C57BL/6N Mice on High-Fat Diet Despite Major Changes in Hepatic One-Carbon Metabolism

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
Author(s):  
Christoph Dahlhoff ◽  
Charles Desmarchelier ◽  
Manuela Sailer ◽  
Rainer W. Fürst ◽  
Alexander Haag ◽  
...  
Keyword(s):  
Carbon Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
One Carbon Metabolism

scholarly journals Hepatic Methionine Homeostasis Is Conserved in C57BL/6N Mice on High-Fat Diet Despite Major Changes in Hepatic One-Carbon Metabolism

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e57387 ◽  
Author(s):  
Christoph Dahlhoff ◽  
Charles Desmarchelier ◽  
Manuela Sailer ◽  
Rainer W. Fürst ◽  
Alexander Haag ◽  
...  
Keyword(s):  
Carbon Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
One Carbon Metabolism

Effects of dietary n-3 PUFA levels in early life on susceptibility to high-fat-diet-induced metabolic syndrome in adult mice

2020 ◽  
pp. 108578
Author(s):  
Dan-Dan Wang ◽  
Fang Wu ◽  
Ling-Yu Zhang ◽  
Ying-Cai Zhao ◽  
Cheng-Cheng Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Early Life ◽  
High Fat ◽  
Adult Mice

scholarly journals High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer’s Disease Signatures

2021 ◽  
Vol 22 (7) ◽  
pp. 3746
Author(s):  
Ilaria Zuliani ◽  
Chiara Lanzillotta ◽  
Antonella Tramutola ◽  
Eugenio Barone ◽  
Marzia Perluigi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Mitochondrial Activity ◽  
High Fat ◽  
Hexosamine Biosynthetic Pathway ◽  
Neurodegenerative Process ◽  
The Brain

The disturbance of protein O-GlcNAcylation is emerging as a possible link between altered brain metabolism and the progression of neurodegeneration. As observed in brains with Alzheimer’s disease (AD), flaws of the cerebral glucose uptake translate into reduced protein O-GlcNAcylation, which promote the formation of pathological hallmarks. A high-fat diet (HFD) is known to foster metabolic dysregulation and insulin resistance in the brain and such effects have been associated with the reduction of cognitive performances. Remarkably, a significant role in HFD-related cognitive decline might be played by aberrant protein O-GlcNAcylation by triggering the development of AD signature and mitochondrial impairment. Our data support the impairment of total protein O-GlcNAcylation profile both in the brain of mice subjected to a 6-week high-fat-diet (HFD) and in our in vitro transposition on SH-SY5Y cells. The reduction of protein O-GlcNAcylation was associated with the development of insulin resistance, induced by overfeeding (i.e., defective insulin signaling and reduced mitochondrial activity), which promoted the dysregulation of the hexosamine biosynthetic pathway (HBP) flux, through the AMPK-driven reduction of GFAT1 activation. Further, we observed that a HFD induced the selective impairment of O-GlcNAcylated-tau and of O-GlcNAcylated-Complex I subunit NDUFB8, thus resulting in tau toxicity and reduced respiratory chain functionality respectively, highlighting the involvement of this posttranslational modification in the neurodegenerative process.

Sign in / Sign up

Export Citation Format

Share Document