Methylation and Expression of Immune and Inflammatory Genes in the Offspring of Bariatric Bypass Surgery Patients

Guénard, Frédéric; Tchernof, André; Deshaies, Yves; Cianflone, Katherine; Kral, John G.; Marceau, Picard; Vohl, Marie‐Claude

doi:10.1155/2013/492170

Cited by 59 publications

(50 citation statements)

References 49 publications

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“…Target genes were identified using a web-based gene network and functional annotation tool (genemania.org/) and review of prior human studies investigating the genetic and epigenetic control of inflammation (30,48,(67)(68)(69)(70) (additional details on target gene selection are provided in SI Materials and Methods). A total of 249 target genes were identified.…”

Section: Methodsmentioning

confidence: 99%

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood

McDade

Ryan

Jones

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

116

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Chronic inflammation contributes to a wide range of human diseases, and environments in infancy and childhood are important determinants of inflammatory phenotypes. The underlying biological mechanisms connecting early environments with the regulation of inflammation in adulthood are not known, but epigenetic processes are plausible candidates. We tested the hypothesis that patterns of DNA methylation (DNAm) in inflammatory genes in young adulthood would be predicted by early life nutritional, microbial, and psychosocial exposures previously associated with levels of inflammation. Data come from a population-based longitudinal birth cohort study in metropolitan Cebu, the Philippines, and DNAm was characterized in whole blood samples from 494 participants (age 20–22 y). Analyses focused on probes in 114 target genes involved in the regulation of inflammation, and we identified 10 sites across nine genes where the level of DNAm was significantly predicted by the following variables: household socioeconomic status in childhood, extended absence of a parent in childhood, exposure to animal feces in infancy, birth in the dry season, or duration of exclusive breastfeeding. To evaluate the biological significance of these sites, we tested for associations with a panel of inflammatory biomarkers measured in plasma obtained at the same age as DNAm assessment. Three sites predicted elevated inflammation, and one site predicted lower inflammation, consistent with the interpretation that levels of DNAm at these sites are functionally relevant. This pattern of results points toward DNAm as a potentially important biological mechanism through which developmental environments shape inflammatory phenotypes across the life course.

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Section: Methodsmentioning

confidence: 99%

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood

McDade

Ryan

Jones

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

116

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“…Epigenetic modifications, such as DNA methylation, might partly mediate associations between maternal and offspring phenotypes by causing changes to gene expression that are mitotically heritable (6,(13)(14)(15). Differential DNA methylation has been reported when assessing offspring exposed in utero to extreme maternal undernutrition (16)(17)(18)(19), maternal morbid obesity (20) and less extreme maternal underweight and maternal obesity (21), in comparison to those not exposed; yet weak or no evidence has been found for associations between continuous maternal BMI and offspring DNA methylation, whether globally (22,23), at specific loci identified in array (21,24,25) or at candidate genes (26). However, individual studies were limited in sample size and thus underpowered to detect differential methylation.…”

Section: Introductionmentioning

confidence: 99%

Maternal BMI at the start of pregnancy and offspring epigenome-wide DNA methylation: Findings from the Pregnancy and Childhood Epigenetics (PACE) consortium

Sharp

Salas²,

Monnereau³

et al. 2017

Preprint

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Pre-pregnancy maternal obesity is associated with adverse offspring outcomes at birth and later in life. Individual studies have shown that epigenetic modifications such as DNA methylation could contribute. Within the Pregnancy and Childhood Epigenetics (PACE) Consortium, we meta-analysed the association between pre-pregnancy maternal BMI and methylation at over 450,000 sites in newborn blood DNA, across 19 cohorts (9,340 mother-newborn pairs). We attempted to infer causality by comparing the effects of maternal versus paternal BMI and incorporating genetic variation. In four additional cohorts (1,817 mother-child pairs), we meta-analysed the association between maternal BMI at the start of pregnancy and blood methylation in adolescents. In newborns, maternal BMI was associated with small (<0.2% per BMI unit (1 kg/m 2 ), P < 1.06 Â 10 À7 ) methylation variation at 9,044 sites throughout the genome. Adjustment for estimated cell proportions greatly attenuated the number of significant CpGs to 104, including 86 sites common to the unadjusted model. At 72/86 sites, the direction of the association was the same in newborns and adolescents, suggesting persistence of signals. However, we found evidence for a6causal intrauterine effect of maternal BMI on newborn methylation at just 8/86 sites. In conclusion, this well-powered analysis identified robust associations between maternal adiposity and variations in newborn blood DNA methylation, but these small effects may be better explained by genetic or lifestyle factors than a causal intrauterine mechanism. This highlights the need for large-scale collaborative approaches and the application of causal inference techniques in epigenetic epidemiology.

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“…Reduced serum adiponectin levels, and increased weights, homeostatic model assessment of insulin resistance, serum retinol binding protein-4 levels, and leptin levels Altered expression of insulin signaling genes in the liver, muscle, and adipose tissues www.global-challenges.com Exercise/weight loss Human/ cohort study Three to six month exercise in men [233,234] Differential methylation of 7663 genes, including 18 obesity-related genes Global and genome-wide sperm DNA methylation changes in genes related to diseases like schizophrenia and Parkinson's disease Human/ cohort study Differences in methylation levels among children born to the same women before and after weight loss due to bariatric surgery [237,[239][240][241] Lower birth weight, and decreased childhood obesity, insulin resistance, cholesterol, leptin and CRP in offsprings born after weight loss…”

Section: Hypomethylation Of the Pancreatic Il13ra2 Genementioning

confidence: 99%

“…[233] These and other epigenetic alterations induced by exercise may be the basis for the reduced risk of obesity in children of women who exercise during pregnancy. [51] Furthermore, exercise is known for reducing weight, and weight loss has important implications on DNA methylation levels, [237][238][239][240][241] which may be mediated via changes in germ cell methylation levels ( Table 2). [234] Overall, the declining levels of physical activity and increasing sedentary lifestyles are likely contributing factors to the growing burden of global NCCDs across successive generations since evidence exists of the transgenerational effects of obesity and exercise.…”

Section: Technological Advances and Physical Activity Levelsmentioning

confidence: 99%

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

Imam

Ismail

2017

Global Challenges

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There are already extensive reviews on the global burden of NCCDs in the public domain. [1][2][3][4][5][6] The consensus that can be surmised from the available data on NCCDs is that their overall prevalence appears to be rising globally and the projections indicate an upward trend. Epidemiological transition data suggests that the morbidity and mortality rate from these diseases is far more than that of communicable diseases in the developed world [7] and a similar trend is now occurring in the low to medium income countries (LMICs). [8] Among the NCCDs, cardiovascular diseases (CVDs) are the leading causes of morbidity and mortality, followed closely by metabolic diseases like Noncommunicable chronic diseases (NCCDs) are the leading causes of morbidity and mortality globally. The mismatch between present day diets and ancestral genome is suggested to contribute to the NCCDs burden, which is promoted by traditional risk factors like unhealthy diets, physical inactivity, alcohol and tobacco. However, epigenetic evidence now suggests that cumulatively inherited epigenetic modifications may have made humans more prone to the effects of present day lifestyle factors. Perinatal starvation was widespread in the 19th century. This together with more recent events like increasing consumption of western and low fiber diets, smoking, harmful use of alcohol, physical inactivity, and environmental pollutants may have programed the human epigenome for higher NCCDs risk. In this review, on the basis of available epigenetic data it is hypothesized that transgenerational effects of lifestyle factors may be contributing to the current global burden of NCCDs. Thus, there is a need to reconsider prevention strategies so that the subsequent generations will not have to pay for our sins and those of our ancestors. Cardiovascular DiseasesDr. M. U. Imam

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Methylation and Expression of Immune and Inflammatory Genes in the Offspring of Bariatric Bypass Surgery Patients

Cited by 59 publications

References 49 publications

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood

Maternal BMI at the start of pregnancy and offspring epigenome-wide DNA methylation: Findings from the Pregnancy and Childhood Epigenetics (PACE) consortium

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

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