Hepatic global DNA Hypomethylation Phenotype in Rainbow Trout Fed Diets Varying in Carbohydrate to Protein Ratio

2021 ◽  
Author(s):  
Jingwei Liu ◽  
Cécile Heraud ◽  
Vincent Véron ◽  
Jésabel Laithier ◽  
Christine Burel ◽  
...  
Keyword(s):  
Dna Demethylation ◽  
Dna Hypomethylation ◽  
Protein Ratio ◽  
High Carbohydrate ◽  
Low Protein ◽  
Demethylation Pathway ◽  
Feeding Trials ◽  
Underlying Mechanisms ◽  
Juvenile Males ◽  
One Way Anova

Abstract Background A high carbohydrate-low protein diet can induce hepatic global DNA hypomethylation in trout. The mechanisms remain unclear. Objective We aimed to investigate whether increase in dietary carbohydrates (dHC) or decrease in dietary proteins (dLP) can cause hepatic global DNA hypomethylation, and to explore the underlying mechanisms in trout. Methods Two feeding trials were conducted on juvenile males, both of which involved a 4-day fasting and 4-day refeeding protocol. In Trial 1, trout were fed either a high protein-no carbohydrate (HP-NC, protein 60% dry matter (DM), carbohydrates 0% DM) or a moderate protein-high carbohydrate (MP-HC, protein 40% DM, carbohydrates 30% DM) diet. In Trial 2, fish were fed either a moderate protein-no carbohydrate (MP-NC, protein 40% DM, carbohydrates 0% DM), a MP-HC (protein 40% DM, carbohydrates 30% DM), or a low protein-no carbohydrate (LP-NC, protein 20% DM, carbohydrates 0% DM) diet to separate the effects of dHC and dLP on the hepatic methylome. Global CmCGG methylation, DNA demethylation derivative levels, and mRNA expression of DNA (de)methylation-related genes were measured. Differences were tested by one-way ANOVA when data were normally distributed or by Kruskal-Wallis non-parametric test if not. Results In both trails, global CmCGG methylation levels remained unaffected, but the hepatic 5-mdC content decreased after refeeding (1–3%). The MP-HC group had 3.4-fold higher hepatic 5-hmdC and a similar 5-mdC level compared to the HP-NC group in Trial 1. Both MP-HC and LP-NC diets lowered the hepatic 5-mdC content (1–2%), but only the LP-NC group had a significantly lower 5-hmdC level (P < 0.01) compared with MP-NC group in Trail 2. Conclusions dHC and dLP independently induced hepatic global DNA demethylation in trout. The alterations in other methylation derivatives levels indicated the demethylation process was achieved through an active demethylation pathway and probably occurred at non-CmCGG sites.

scholarly journals The chromosomal protein SMCHD1 regulates DNA methylation and the 2c-like state of embryonic stem cells by antagonizing TET proteins

2021 ◽  
Vol 7 (4) ◽  
pp. eabb9149
Author(s):  
Zhijun Huang ◽  
Jiyoung Yu ◽  
Wei Cui ◽  
Benjamin K. Johnson ◽  
Kyunggon Kim ◽  
...  
Keyword(s):  
Es Cells ◽  
Embryonic Stem ◽  
Homeobox Gene ◽  
Dna Demethylation ◽  
Chromosomal Protein ◽  
Dna Hypomethylation ◽  
Tet Proteins ◽  
Target Sites ◽  
Structural Maintenance Of Chromosomes ◽  
Hinge Domain

5-Methylcytosine (5mC) oxidases, the ten-eleven translocation (TET) proteins, initiate DNA demethylation, but it is unclear how 5mC oxidation is regulated. We show that the protein SMCHD1 (structural maintenance of chromosomes flexible hinge domain containing 1) is found in complexes with TET proteins and negatively regulates TET activities. Removal of SMCHD1 from mouse embryonic stem (ES) cells induces DNA hypomethylation, preferentially at SMCHD1 target sites and accumulation of 5-hydroxymethylcytosine (5hmC), along with promoter demethylation and activation of the Dux double-homeobox gene. In the absence of SMCHD1, ES cells acquire a two-cell (2c) embryo–like state characterized by activation of an early embryonic transcriptome that is substantially imposed by Dux. Using Smchd1/Tet1/Tet2/Tet3 quadruple-knockout cells, we show that DNA demethylation, activation of Dux, and other genes upon SMCHD1 loss depend on TET proteins. These data identify SMCHD1 as an antagonist of the 2c-like state of ES cells and of TET-mediated DNA demethylation.

Effect of High-Salt, High-Carbohydrate, Low-Protein Diet on Hypertension in the Rat

1973 ◽  
Vol 45 (s1) ◽  
pp. 99s-102s
Author(s):  
Hideo Ueda
Keyword(s):  
Blood Pressure ◽  
High Protein Diet ◽  
Normal Diet ◽  
High Salt ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Heart Weight ◽  
Hypertensive Rats ◽  
High Carbohydrate ◽  
Low Protein

1. High-salt, high-carbohydrate and low-protein diet induces remarkable elevation of blood pressure in spontaneous hypertensive rats (SHR). 2. These animals have low serum potassium, low blood urea nitrogen and high blood sugar. 3. Heart weight is increased in proportion to the elevation of blood pressure. 4. Kidney weight of rats receiving the high-salt, high-carbohydrate and low-protein diet was, by contrast, smaller than SHR receiving a normal diet. 5. The kidneys of SHR receiving a high-salt, high-protein diet were twice as heavy as the kidneys of normal rats. 6. Similar dietary modifications in Goldblatt hypertensive rats to those in SHR produced similar changes in blood pressure and heart weight.

scholarly journals A low-protein, high-carbohydrate diet increases de novo fatty acid synthesis from glycerol and glycerokinase content in the liver of growing rats

2013 ◽  
Vol 33 (6) ◽  
pp. 494-502 ◽  
Author(s):  
Andreza Lúcia Menezes ◽  
Mayara Peron Pereira ◽  
Samyra Lopes Buzelle ◽  
Maísa Pavani dos Santos ◽  
Suélem Aparecida de França ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Growing Rats ◽  
Low Protein

Low-protein, high-carbohydrate diet increases glucose uptake and fatty acid synthesis in brown adipose tissue of rats

Nutrition ◽  
2014 ◽  
Vol 30 (4) ◽  
pp. 473-480 ◽  
Author(s):  
Suélem Aparecida de França ◽  
Maísa Pavani dos Santos ◽  
Roger Vinícius Nunes Queiroz da Costa ◽  
Mendalli Froelich ◽  
Samyra Lopes Buzelle ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Protein ◽  
Brown Adipose

A Low-Protein, High-Carbohydrate Diet Stimulates Thermogenesis in the Brown Adipose Tissue of Rats via ATF-2

Lipids ◽  
2016 ◽  
Vol 51 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Suélem A. de França ◽  
Maísa P. dos Santos ◽  
Franciele Przygodda ◽  
Maria Antonieta R. Garófalo ◽  
Isis C. Kettelhut ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Protein ◽  
Brown Adipose

The impact of low-protein high-carbohydrate diets on aging and lifespan

2015 ◽  
Vol 73 (6) ◽  
pp. 1237-1252 ◽  
Author(s):  
David G. Le Couteur ◽  
Samantha Solon-Biet ◽  
Victoria C. Cogger ◽  
Sarah J. Mitchell ◽  
Alistair Senior ◽  
...  
Keyword(s):  
High Carbohydrate ◽  
Low Protein ◽  
The Impact

scholarly journals Periodized low protein-high carbohydrate diet confers potent, but transient, metabolic improvements

2018 ◽  
Vol 17 ◽  
pp. 112-121 ◽  
Author(s):  
Zhencheng Li ◽  
Mette Line Rasmussen ◽  
Jingwen Li ◽  
Carlos Henriquez-Olguin ◽  
Jonas Roland Knudsen ◽  
...  
Keyword(s):  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Protein

scholarly journals Paternal diet programs offspring health through sperm- and seminal plasma-specific pathways in mice

2018 ◽  
Vol 115 (40) ◽  
pp. 10064-10069 ◽  
Author(s):  
Adam J. Watkins ◽  
Irundika Dias ◽  
Heather Tsuro ◽  
Danielle Allen ◽  
Richard D. Emes ◽  
...  
Keyword(s):  
Seminal Plasma ◽  
Semen Quality ◽  
Protein Diet ◽  
Male Mating ◽  
Adult Offspring ◽  
Nonalcoholic Fatty Liver ◽  
Low Protein ◽  
Specific Effects ◽  
Underlying Mechanisms ◽  
Offspring Health

The association between poor paternal diet, perturbed embryonic development, and adult offspring ill health represents a new focus for the Developmental Origins of Health and Disease hypothesis. However, our understanding of the underlying mechanisms remains ill-defined. We have developed a mouse paternal low-protein diet (LPD) model to determine its impact on semen quality, maternal uterine physiology, and adult offspring health. We observed that sperm from LPD-fed male mice displayed global hypomethylation associated with reduced testicular expression of DNA methylation and folate-cycle regulators compared with normal protein diet (NPD) fed males. Furthermore, females mated with LPD males display blunted preimplantation uterine immunological, cell signaling, and vascular remodeling responses compared to controls. These data indicate paternal diet impacts on offspring health through both sperm genomic (epigenetic) and seminal plasma (maternal uterine environment) mechanisms. Extending our model, we defined sperm- and seminal plasma-specific effects on offspring health by combining artificial insemination with vasectomized male mating of dietary-manipulated males. All offspring derived from LPD sperm and/or seminal plasma became heavier with increased adiposity, glucose intolerance, perturbed hepatic gene expression symptomatic of nonalcoholic fatty liver disease, and altered gut bacterial profiles. These data provide insight into programming mechanisms linking poor paternal diet with semen quality and offspring health.

Sign in / Sign up

Export Citation Format

Share Document