A systematic review of studies of DNA methylation in the context of a weight loss intervention

Aronica, Lucia; Levine, A. Joan; Brennan, Kevin; Mi, Jeffrey; Gardner, Christopher D.; Haile, Robert W.; Hitchins, Megan P.

doi:10.2217/epi-2016-0182

Cited by 42 publications

(39 citation statements)

References 58 publications

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“…An emerging hypothesis is that epigenetic factors might help explain some of the remaining variability in BMI between people by mediating the interaction between genetic factors and environmental factors. Indeed, recent studies suggest that epigenetic markers, in particular DNAm biomarkers, are more strongly associated with BMI and obesity traits than genetic sequence variants . This is in line with what we know about epigenetic memory—the ability of the epigenome to store a molecular memory of our lifestyle exposure.…”

Section: Epigenetics and Personalized Healthsupporting

confidence: 59%

“…A few clinical trials show that it is possible to measure DNAm at specific genes before a diet intervention and predict whether someone is going to lose weight on a certain diet. Strikingly, many of these DNAm biomarkers are located in proximity to metabolic or obesity‐associated genes such as leptin , Tumor necrosis factor‐alpha , Brain Derived neurotrophic factor , and Neuropeptide‐Y …”

Section: Epigenetics and Personalized Healthmentioning

confidence: 99%

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RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

Skinner

Lumey

Fleming

et al. 2019

J Parenter Enteral Nutr

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The goal of the 2018 American Society for Parenteral and Enteral Nutrition (ASPEN) Research Workshop was to explore the influence of nutrition and dietary exposure to xenobiotics on the epigenome during critical periods in development and how these exposures influence both disease incidence and severity transgenerationally. A growing compendium of research indicates that the incidence and severity of common and costly human diseases may be influenced by dietary exposures and deficiencies that modify the epigenome. The greatest periods of vulnerability to these exposures are the periconception period and early childhood. Xenobiotics in the food chain, protein malnutrition, and methyl donor deficiencies could have a profound bearing on the risk of developing heart disease, diabetes, obesity, hypertension, and mental illness over multiple generations. The financial impact and the life burden of these diseases are enormous. These and other aspects of nutrition, epigenetics, and health are explored in this research workshop.

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Section: Epigenetics and Personalized Healthsupporting

confidence: 59%

Section: Epigenetics and Personalized Healthmentioning

confidence: 99%

RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

Skinner

Lumey

Fleming

et al. 2019

J Parenter Enteral Nutr

Self Cite

View full text Add to dashboard Cite

show abstract

“…A clinically relevant aspect of such studies relates to the context of weight loss and whether the effects of dietary challenge and obesity remain. In human surveys of DNA methylation during weight loss, it was observed that modest but widespread changes to DNA methylation were found near known obesity and diabetes genes in liver and adipose (13). Other studies identified DNA methylation differences near known obesity genes predicting high or low responses to therapies like caloric restriction, exercise, or surgical interventions (14)(15)(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

DNA Methylation Changes More Slowly Than Physiological States in Response to Weight Loss in Genetically Diverse Mouse Strains

et al. 2019

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Responses to a high fat, high sucrose (HFHS) diet vary greatly among inbred strains of mice. We sought to examine the epigenetic (DNA methylation) changes underlying these differences as well as variation in weight loss when switched to a low-fat chow diet. We surveyed DNA methylation from livers of 45 inbred mouse strains fed a HFHS diet for 8 weeks using reduced-representation bisulfite sequencing (RRBS). We observed a total of 1,045,665 CpGs of which 83 candidate sites were significantly associated with HFHS diet. Many of these CpGs correlated strongly with gene expression or clinical traits such as body fat percentage and plasma glucose. Five inbred strains were then studied in the context of weight loss to test for evidence of epigenetic "memory." The mice were first fed a HFHS diet for 6 weeks followed by a low-fat chow diet for 4 weeks. Four of the five strains returned to initial levels of body fat while one strain, A/J, retained almost 50% of the fat gained. A total of 36 of the HFHS diet responsive CpGs exhibited evidence of persistent epigenetic modifications following weight normalization, including CpGs near the genes Scd1 and Cdk1. Our study identifies DNA methylation changes in response to a HFHS diet challenge that revert more slowly than overall body fat percentage in weight loss and provides evidence for epigenetic mediated "memory."

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“…tobacco) 6 . An obesogenic environment may comprise factors that induce inappropriate expression or silencing of genes leading to metabolic imbalances that trigger obesity development 7 . Furthermore, the stress caused by obesity may require metabolic changes to help the body to cope.…”

Section: Introductionmentioning

confidence: 99%

Epigenome-wide methylation differences in a group of lean and obese women – A HUNT Study

Kvaløy

Page

Holmen

2018

Sci Rep

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Knowledge of epigenetically regulated biomarkers linked to obesity development is still scarce. Improving molecular understanding of the involved factors and pathways would improve obesity phenotype characterization and reveal potentially relevant targets for obesity intervention. The Illumina Infinium HumanMethylation450 BeadChip was used in a leucocyte epigenome-wide association study (EWAS) to quantify differential DNA methylation in 60 lean compared with 60 obese young women. Replication was done in monozygotic twins discordant for obesity. At adolescence and adulthood, the two weight groups differed significantly in obesity-related traits and metabolic risk factors. Differential hypomethylation was overrepresented in obese compared to lean women. In the adjusted model, the EWAS revealed 10 differentially methylated CpG sites linked to 8 gene loci – COX6A1P2/FGD2, SBNO2, TEX41, RPS6KA2, IGHE/IGHG1/IGHD, DMAP1, SOCS3, and SETBP1– and an enhancer locus at chromosome 2 (2p25.1). The sites linked to TEX41, IGHE/IGHG1/IGHD, DMAP1, and SETBP1 were novel findings, while COX6A1P/FGD2, SBNO2, RPS6KA2, and SOCS3 had been identified previously with concordant direction of effects. RPS6KA2, DMAP1, and SETBP1 were replicated in the BMI-discordant monozygotic twin cohort using the FDR of 5%.

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A systematic review of studies of DNA methylation in the context of a weight loss intervention

Abstract: The identified weight loss associated DNAm markers, especially those showing reproducibility across different studies, warrant validation by further studies with robust design and adequate power.

Cited by 42 publications

References 58 publications

RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

DNA Methylation Changes More Slowly Than Physiological States in Response to Weight Loss in Genetically Diverse Mouse Strains

Epigenome-wide methylation differences in a group of lean and obese women – A HUNT Study

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