scholarly journals DNA Methylation Pattern in Overweight Women under an Energy-Restricted Diet Supplemented with Fish Oil

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Cátia Lira do Amaral ◽  
Fermín I. Milagro ◽  
Rui Curi ◽  
J. Alfredo Martínez
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Weight Loss ◽  
Fish Oil ◽  
Mononuclear Cells ◽  
Energy Restriction ◽  
Dietary Factors ◽  
Epigenetic Mechanisms ◽  
Overweight Women ◽  
Fish Oil Supplementation

Dietary factors modulate gene expression and are able to alter epigenetic signatures in peripheral blood mononuclear cells (PBMC). However, there are limited studies about the effects of omega-3 polyunsaturated fatty acids (n-3 PUFA) on the epigenetic mechanisms that regulate gene expression. This research investigates the effects ofn-3-rich fish oil supplementation on DNA methylation profile of several genes whose expression has been reported to be downregulated byn-3 PUFA in PBMC:CD36,FFAR3,CD14,PDK4, andFADS1. Young overweight women were supplemented with fish oil or control in a randomized 8-week intervention trial following a balanced diet with 30% energy restriction. Fatty acid receptorCD36decreased DNA methylation at CpG +477 due to energy restriction. Hypocaloric diet-induced weight loss also reduced the methylation percentages of CpG sites located inCD14,PDK4, andFADS1. The methylation patterns of these genes were only slightly affected by the fish oil supplementation, being the most relevant to the attenuation of the weight loss-induced decrease inCD36methylation after adjusting by baseline body weight. These results suggest that then-3 PUFA-induced changes in the expression of these genes in PBMC are not mediated by DNA methylation, although other epigenetic mechanisms cannot be discarded.

scholarly journals Fish-oil supplementation induces antiinflammatory gene expression profiles in human blood mononuclear cells

2009 ◽  
Vol 90 (2) ◽  
pp. 415-424 ◽  
Author(s):  
Mark Bouwens ◽  
Ondine van de Rest ◽  
Neele Dellschaft ◽  
Mechteld Grootte Bromhaar ◽  
Lisette CPGM de Groot ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fish Oil ◽  
Human Blood ◽  
Mononuclear Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Blood Mononuclear Cells ◽  
Fish Oil Supplementation

scholarly journals DNA methylation and retinal degenerative diseases: at the crossroad between genes and diet

2020 ◽  
Vol 53 (383) ◽  
pp. MISC1-MISC3
Author(s):  
Andrea Maugeri
Keyword(s):  
Dna Methylation ◽  
Methylation Level ◽  
Integrated Approach ◽  
Dietary Factors ◽  
Epigenetic Mechanisms ◽  
Degenerative Diseases ◽  
Retinal Cells ◽  
Significant Difference ◽  
Retinal Degenerative Diseases ◽  
The Impact

Retinal degenerative diseases are the leading causes of blindness and low vision among working-age and older adults worldwide, with 170 and 130 million individuals suffering from age-related macular degeneration (AMD) and diabetic retinopathy, respectively. Although several studies began to show benefits from dietary interventions against retinal degenerative disease, an integrated approach is needed to understand molecular mechanisms underpinning the protective or risky effect of dietary factors. A specific area of research that elucidates mechanisms involved in gene-diet interaction is the Nutri-epigenomics, the study of the impact of diet on gene expression by modulating epigenetic mechanisms. The present research investigated the role of DNA methylation – one of the most commonly analysed epigenetic mechanisms - in the pathophysiology of retinal degenerative diseases, by exploiting a multiple integrated approach. In vitro studies initially helped us to understand how pathological features of retinal degeneration (e.g. oxidative stress, inflammation and hyperglycaemia) modulated functions of enzymes involved in the methylation of Long Interspersed Nuclear Element 1 (LINE-1) sequences in retinal cells. We also proved that some nutrients (e.g. resveratrol and curcumin) might counteract these effects and restore DNA methylation level in retinal cells under oxidative, inflammatory and high glucose conditions. We further analysed whether LINE-1 methylation level differed between patients with AMD and controls without posterior segment eye diseases. Interestingly, we noted a significant difference between the two groups, with higher LINE-1 methylation level in blood samples from AMD patients. This evidence -albeit promising for biomarker discovery- requires confirmation by further large-size prospective studies taking into account different factors. Our research, in fact, also suggested that the risk of retinal degenerative diseases derives from the combination of genetic risk variants, clinical characteristics, environmental exposures and unhealthy lifestyles, which in turn are interrelated. Thus, it would be interesting to study how the exposome -the totality of exposures individuals experience over the course of life- might induce epigenetic mechanisms able to reduce or increase the risk for retinal degenerative diseases.

The effect of intermittent energy restriction on weight loss and diabetes risk markers in women with a history of gestational diabetes: a 12-month randomized control trial

2021 ◽  
Author(s):  
Kristy L Gray ◽  
Peter M Clifton ◽  
Jennifer B Keogh
Keyword(s):  
Weight Loss ◽  
Gestational Diabetes ◽  
Serum Insulin ◽  
Dropout Rate ◽  
Energy Restriction ◽  
Diabetes Risk ◽  
Oral Glucose ◽  
Risk Markers ◽  
Overweight Women ◽  
The Mean

ABSTRACT Background Weight loss after gestational diabetes (GDM) can prevent or delay the onset of type 2 diabetes. Intermittent energy restriction (IER) may offer an alternative to continuous energy restriction (CER) for weight loss. Objectives We compared the effects of IER (2 days per week) to daily CER over 12 mo on weight loss and diabetes risk markers in overweight women with previous GDM. Methods Overweight females (n = 121) ≥18 y were randomized 1:1 to either IER [2-d 500 kcal (2100 kJ); n = 61] or CER [1500 kcal (6000 kJ); n = 60] in this 12-mo noninferiority trial. Results The trial was completed by 62 participants with a median age of 39.6 y [Quartile (Q) 1 to Quartile 3, 34.9 to 43.9 y] with a median BMI of 32.6 kg/m2 (Q1 to Q3, 28.5 to 37.9 kg/m2) at a median of 2.9 y after GDM (Q1 to Q3, 2.1 to 6.4 y; 49% attrition; IER n = 29; CER n = 30; P = 0.8). The mean ± SD weight loss was significant over time (P < 0.001) but not by diet group (IER −4.8 ± 5.0 kg; CER −3.2 ± 5.0; P = 0.2). The mean between-group difference was −1.6 kg (95% CI: −4.2 to 1.0 kg; P = 0.2). There were no significant between-group differences in change in HbA1c, fasting plasma glucose, fasting serum insulin, HOMA-IR or 2-h oral glucose tolerance at 12 mo (p>0.05). The trial was registered at https://www.anzctr.org.au/ (ACTRN12617001476325). Conclusions IER produces comparable weight loss to CER over 12 mo in overweight women with previous GDM. The high dropout rate in this study is a limitation in the interpretation of these results. Larger studies are needed to confirm noninferiority of IER compared to CER.

scholarly journals Changes in DNA Methylation and Gene Expression of Insulin and Obesity-Related Gene PIK3R1 after Roux-en-Y Gastric Bypass

2020 ◽  
Vol 21 (12) ◽  
pp. 4476
Author(s):  
Marcela A S Pinhel ◽  
Natália Y Noronha ◽  
Carolina F Nicoletti ◽  
Vanessa AB Pereira ◽  
Bruno AP de Oliveira ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Weight Loss ◽  
Gastric Bypass ◽  
Related Gene ◽  
Cpg Sites ◽  
Genome Wide ◽  
Genetically Determined ◽  
Methylation Patterns ◽  
Weight Loss Interventions

Weight regulation and the magnitude of weight loss after a Roux-en-Y gastric bypass (RYGB) can be genetically determined. DNA methylation patterns and the expression of some genes can be altered after weight loss interventions, including RYGB. The present study aimed to evaluate how the gene expression and DNA methylation of PIK3R1, an obesity and insulin-related gene, change after RYGB. Blood samples were obtained from 13 women (35.9 ± 9.2 years) with severe obesity before and six months after surgical procedure. Whole blood transcriptome and epigenomic patterns were assessed by microarray-based, genome-wide technologies. A total of 1966 differentially expressed genes were identified in the pre- and postoperative periods of RYGB. From these, we observed that genes involved in obesity and insulin pathways were upregulated after surgery. Then, the PIK3R1 gene was selected for further RT-qPCR analysis and cytosine-guanine nucleotide (CpG) sites methylation evaluation. We observed that the PI3KR1 gene was upregulated, and six DNA methylation CpG sites were differently methylated after bariatric surgery. In conclusion, we found that RYGB upregulates genes involved in obesity and insulin pathways.

scholarly journals Fish oil supplementation reverses the effect of cholesterol on apoptotic gene expression in smooth muscle cells

2010 ◽  
Vol 9 (1) ◽  
pp. 70 ◽  
Author(s):  
Sonia Perales ◽  
Ma Alejandre ◽  
Rogelio Morales ◽  
Carolina Torres ◽  
Ana Linares
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Fish Oil ◽  
Muscle Cells ◽  
Apoptotic Gene ◽  
Fish Oil Supplementation

scholarly journals Architectural Epigenetics: Mitotic Retention of Mammalian Transcriptional Regulatory Information

2010 ◽  
Vol 30 (20) ◽  
pp. 4758-4766 ◽  
Author(s):  
Sayyed K. Zaidi ◽  
Daniel W. Young ◽  
Martin Montecino ◽  
Jane B. Lian ◽  
Janet L. Stein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Transcription Factor ◽  
Epigenetic Mechanisms ◽  
Cellular Phenotype ◽  
Transcriptional Regulatory ◽  
Regulatory Information ◽  
Cellular Identity ◽  
Epigenetic Signatures ◽  
Transcription Factor Occupancy

ABSTRACT Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustained cellular identity in progeny cells. We propose that these mitotic epigenetic signatures collectively constitute architectural epigenetics, a novel and essential mechanism that conveys regulatory information to sustain the control of phenotype and proliferation in progeny cells by bookmarking genes for activation or suppression.

scholarly journals Transcriptome-based identification of antioxidative gene expression after fish oil supplementation in normo- and dyslipidemic men

2012 ◽  
Vol 9 (1) ◽  
pp. 45 ◽  
Author(s):  
Simone Schmidt ◽  
Frank Stahl ◽  
Kai-Oliver Mutz ◽  
Thomas Scheper ◽  
Andreas Hahn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fish Oil ◽  
Fish Oil Supplementation

scholarly journals The effect of intermittent energy and carbohydrate restrictionv. daily energy restriction on weight loss and metabolic disease risk markers in overweight women

2013 ◽  
Vol 110 (8) ◽  
pp. 1534-1547 ◽  
Author(s):  
Michelle Harvie ◽  
Claire Wright ◽  
Mary Pegington ◽  
Debbie McMullan ◽  
Ellen Mitchell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Disease Risk ◽  
Phase 1 ◽  
Weight Maintenance ◽  
Energy Restriction ◽  
Overweight Women ◽  
Daily Energy

Intermittent energy restriction may result in greater improvements in insulin sensitivity and weight control than daily energy restriction (DER). We tested two intermittent energy and carbohydrate restriction (IECR) regimens, including one which allowedad libitumprotein and fat (IECR+PF). Overweight women (n115) aged 20 and 69 years with a family history of breast cancer were randomised to an overall 25 % energy restriction, either as an IECR (2500–2717 kJ/d, < 40 g carbohydrate/d for 2 d/week) or a 25 % DER (approximately 6000 kJ/d for 7 d/week) or an IECR+PF for a 3-month weight-loss period and 1 month of weight maintenance (IECR or IECR+PF for 1 d/week). Insulin resistance reduced with the IECR diets (mean − 0·34 (95 % CI − 0·66, − 0·02) units) and the IECR+PF diet (mean − 0·38 (95 % CI − 0·75, − 0·01) units). Reductions with the IECR diets were significantly greater compared with the DER diet (mean 0·2 (95 % CI − 0·19, 0·66) μU/unit,P= 0·02). Both IECR groups had greater reductions in body fat compared with the DER group (IECR: mean − 3·7 (95 % CI − 2·5, − 4·9) kg,P= 0·007; IECR+PF: mean − 3·7 (95 % CI − 2·8, − 4·7) kg,P= 0·019; DER: mean − 2·0 (95 % CI − 1·0, 3·0) kg). During the weight maintenance phase, 1 d of IECR or IECR+PF per week maintained the reductions in insulin resistance and weight. In the short term, IECR is superior to DER with respect to improved insulin sensitivity and body fat reduction. Longer-term studies into the safety and effectiveness of IECR diets are warranted.

scholarly journals Leveraging brain cortex-derived molecular data to elucidate epigenetic and transcriptomic drivers of neurological function and disease

2018 ◽  
Author(s):  
Charlie Hatcher ◽  
Caroline L. Relton ◽  
Tom R. Gaunt ◽  
Tom G. Richardson
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Histone Acetylation ◽  
Genetic Variants ◽  
Large Scale ◽  
Genetic Variant ◽  
Association Studies ◽  
Genome Wide Association Studies ◽  
Epigenetic Mechanisms ◽  
Trait Variation

AbstractIntegrative approaches which harness large-scale molecular datasets can help develop mechanistic insight into findings from genome-wide association studies (GWAS). We have performed extensive analyses to uncover transcriptional and epigenetic processes which may play a role in neurological trait variation.This was undertaken by applying Bayesian multiple-trait colocalization systematically across the genome to identify genetic variants responsible for influencing intermediate molecular phenotypes as well as neurological traits. In this analysis we leveraged high dimensional quantitative trait loci data derived from prefrontal cortex tissue (concerning gene expression, DNA methylation and histone acetylation) and GWAS findings for 5 neurological traits (Neuroticism, Schizophrenia, Educational Attainment, Insomnia and Alzheimer’s disease).There was evidence of colocalization for 118 associations suggesting that the same underlying genetic variant influenced both nearby gene expression as well as neurological trait variation. Of these, 73 associations provided evidence that the genetic variant also influenced proximal DNA methylation and/or histone acetylation. These findings support previous evidence at loci where epigenetic mechanisms may putatively mediate effects of genetic variants on traits, such as KLC1 and schizophrenia. We also uncovered evidence implicating novel loci in neurological disease susceptibility, including genes expressed predominantly in brain tissue such as MDGA1, KIRREL3 and SLC12A5.An inverse relationship between DNA methylation and gene expression was observed more than can be accounted for by chance, supporting previous findings implicating DNA methylation as a transcriptional repressor. Our study should prove valuable in helping future studies prioritise candidate genes and epigenetic mechanisms for in-depth functional follow-up analyses.

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