Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level

2015 ◽  
Vol 129 (4) ◽  
pp. 385-394 ◽  
Author(s):  
Xuemei Xie ◽  
Hongjie Gao ◽  
Wanjiang Zeng ◽  
Suhua Chen ◽  
Ling Feng ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gestational Diabetes ◽  
Glucose Level ◽  
Peroxisome Proliferator ◽  
Diabetes Group ◽  
Peroxisome Proliferator Activated Receptor ◽  
Site Specific ◽  
Cpg Site

Among all the participants, the maternal gestational glucose level was positively correlated with placental DNA methylation. The correlation between gestational 2-h post-OGTT glycaemia and CpG site-specific methylation in placenta was stronger in the gestational diabetes group.

scholarly journals Intensity-Specific Differential Leukocyte DNA Methylation in Physical (In)Activity: An Exploratory Approach

2018 ◽  
Vol 21 (2) ◽  
pp. 101-111 ◽  
Author(s):  
Maarten Caspers ◽  
Sara Blocquiaux ◽  
Ruben Charlier ◽  
Sara Knaeps ◽  
Johan Lefevre ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Correlation Coefficients ◽  
Global Dna Methylation ◽  
Site Specific ◽  
Cpg Sites ◽  
Cpg Site ◽  
Biological Pathway Analysis ◽  
Exploratory Approach ◽  
Health Related ◽  
Related Pathway

The aim of this exploratory study was to investigate how sedentary behavior (SB) and physical activity (PA) influence DNA methylation at a global, gene-specific, and health-related pathway level. SB, light PA (LPA), and moderate-to-vigorous PA (MVPA) were assessed objectively for 41 Flemish men using the SenseWear Pro 3 Armband. CpG site-specific methylation in leukocytes was determined using the Illumina HumanMethylation 450 BeadChip. Correlations were calculated between time spent on the three PA intensity levels and global DNA methylation, using a z-score-based method to determine global DNA methylation levels. To determine whether CpG site-specific methylation can be predicted by these three PA intensity levels, linear regression analyses were performed. Based on the significantly associated CpG sites at α = 0.005, lists were created including all genes with a promoter region overlapping these CpG sites. A biological pathway analysis determined to what extent these genes are overrepresented within several pathways. No significant associations were observed between global DNA methylation and SB (r = 0.084), LPA (r = -0.168), or MVPA (r = -0.125), although the direction of the correlation coefficients is opposite to what is generally reported in literature. SB has a different impact on global and gene-specific methylation than PA, but also LPA and MVPA affect separate genes and pathways. Furthermore, the function of a pathway seems to determine its association with SB, LPA, or MVPA. Multiple PA intensity levels, including SB, should be taken into account in future studies investigating the effect of physical (in)activity on human health through epigenetic mechanisms.

scholarly journals Sleep duration and fragmentation in relation to leukocyte DNA methylation in adolescents

SLEEP ◽  
2019 ◽  
Vol 42 (9) ◽  
Author(s):  
Erica C Jansen ◽  
Dana C Dolinoy ◽  
Louise M O’Brien ◽  
Karen E Peterson ◽  
Ronald D Chervin ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Sleep Duration ◽  
Epigenetic Modification ◽  
Sleep Fragmentation ◽  
Peroxisome Proliferator ◽  
Inverse Association ◽  
Blood Leukocytes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Movement Index ◽  
Candidate Regions

Abstract Study Objectives Sleep deprivation and low sleep quality are widespread among adolescents, and associate with obesity risk. Plausible mediators include diet and physical activity. Another potential interrelated pathway, as yet unexplored in adolescents, could involve epigenetic modification of metabolism genes. Methods In a cohort of 351 Mexico City adolescents (47% male; mean [SD] age = 14 [2] years), 7-day actigraphy was used to assess average sleep duration, sleep fragmentation, and movement index. DNA isolated from blood leukocytes was bisulfite-converted, amplified, and pyrosequenced at four candidate regions. Linear mixed models evaluated sex-stratified associations between sleep characteristics (split into quartiles [Q]) and DNA methylation of each region, adjusted for potential confounders. Results Mean sleep duration was 8.5 [0.8] hours for boys and 8.7 [1] hours for girls. There were sex-specific associations between sleep duration and LINE-1 (long interspersed nuclear element) methylation. Boys with longer sleep duration (Q4) had lower LINE-1 methylation than boys in the 3rd quartile reference category, while girls with both longer and shorter sleep duration had higher LINE-1 methylation compared to Q3. Longer sleep duration was associated with higher H19 methylation among girls (comparing highest to third quartile, −0.9% [−2.2, 0.5]; p, trend = 0.047). Sleep fragmentation was inversely associated with peroxisome proliferator-activated receptor alpha (PPARA) methylation among girls (comparing highest to lowest fragmentation quartile, 0.9% [0.1 to 1.8]). Girls also showed an inverse association between sleep fragmentation and hydroxysteroid (11-beta) dehydrogenase 2 (HSD11B2; Q4 to Q1, 0.6% [−1.2%, 0%]). Conclusions Sleep duration and fragmentation in adolescents show sex-specific associations with leukocyte DNA methylation patterns of metabolism genes.

Differential methylation of insulin-like growth factor 2 in offspring of physically active pregnant women

2018 ◽  
Vol 9 (3) ◽  
pp. 299-306 ◽  
Author(s):  
M. R. Marshall ◽  
N. Paneth ◽  
J. A. Gerlach ◽  
L. M. Mudd ◽  
L. Biery ◽  
...  
Keyword(s):  
Physical Activity ◽  
Dna Methylation ◽  
Growth Factor ◽  
Candidate Gene ◽  
Pyruvate Dehydrogenase Kinase ◽  
Peroxisome Proliferator ◽  
Insulin Like Growth Factor ◽  
Gene Methylation ◽  
Global Methylation ◽  
Peroxisome Proliferator Activated Receptor

AbstractSeveral studies have suggested that maternal lifestyle during pregnancy may influence long-term health of offspring by altering the offspring epigenome. Whether maternal leisure-time physical activity (LTPA) during pregnancy might have this effect is unknown. The purpose of this study was to determine the relationship between maternal LTPA during pregnancy and offspring DNA methylation. Participants were recruited from the Archive for Research on Child Health study. At enrollment, participants’ demographic information and self-reported LTPA during pregnancy were determined. High active participants (averaged 637.5 min per week of LTPA; n=14) were matched by age and race to low active participants (averaged 59.5 min per week LTPA; n=28). Blood spots were obtained at birth. Pyrosequencing was used to determine methylation levels of long interspersed nucleotide elements (LINE-1) (global methylation) and peroxisome proliferator-activated receptor-gamma (PPARγ), peroxisome proliferator-activated receptor-gamma coactivator (PGC1-α), insulin-like growth factor 2 (IGF2), pyruvate dehydrogenase kinase, isozyme 4 (PDK4) and transcription factor 7-like 2 (TCF7L2). We found no differences between offspring of high active and low active groups for LINE-1 methylation. The only differences in candidate gene methylation between groups were at two CpG sites in the P2 promoter of IGF2; the offspring of low active group had significantly higher DNA methylation (74.70±2.25% methylation for low active v. 72.83±2.85% methylation for high active; P=0.045). Our results suggest no effect of maternal LTPA on offspring global and candidate gene methylation, with the exception of IGF2. IGF2 has been previously associated with regulation of physical activity, suggesting a possible role of maternal LTPA on regulation of offspring physical activity.

scholarly journals Deoxyribonucleic Acid Methylation and Gene Expression of PPARGC1A in Human Muscle Is Influenced by High-Fat Overfeeding in a Birth-Weight-Dependent Manner

2010 ◽  
Vol 95 (6) ◽  
pp. 3048-3056 ◽  
Author(s):  
Charlotte Brøns ◽  
Stine Jacobsen ◽  
Emma Nilsson ◽  
Tina Rönn ◽  
Christine B. Jensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Dna Methylation ◽  
Birth Weight ◽  
Control Diet ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Peripheral Insulin Resistance

Abstract Context: Low birth weight (LBW) and unhealthy diets are risk factors of metabolic disease including type 2 diabetes (T2D). Genetic, nongenetic, and epigenetic data propose a role of the key metabolic regulator peroxisome proliferator-activated receptor γ, coactivator 1α (PPARGC1A) in the development of T2D. Objective: Our objective was to investigate gene expression and DNA methylation of PPARGC1A and coregulated oxidative phosphorylation (OXPHOS) genes in LBW and normal birth weight (NBW) subjects during control and high-fat diets. Design, Subjects, and Main Outcome Measures: Twenty young healthy men with LBW and 26 matched NBW controls were studied after 5 d high-fat overfeeding (+50% calories) and after a control diet in a randomized manner. Hyperinsulinemic-euglycemic clamps were performed and skeletal muscle biopsies excised. DNA methylation and gene expression were measured using bisulfite sequencing and quantitative real-time PCR, respectively. Results: When challenged with high-fat overfeeding, LBW subjects developed peripheral insulin resistance and reduced PPARGC1A and OXPHOS (P < 0.05) gene expression. PPARGC1A methylation was significantly higher in LBW subjects (P = 0.0002) during the control diet. However, PPARGC1A methylation increased in only NBW subjects after overfeeding in a reversible manner. DNA methylation of PPARGC1A did not correlate with mRNA expression. Conclusions: LBW subjects developed peripheral insulin resistance and decreased gene expression of PPARGC1A and OXPHOS genes when challenged with fat overfeeding. The extent to which our finding of a constitutively increased DNA methylation in the PPARGC1A promoter in LBW subjects may contribute needs to be determined. We provide the first experimental support in humans that DNA methylation induced by overfeeding is reversible.

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