Subtle decreases in DNA methylation and gene expression at the mouse Igf2 locus following prenatal alcohol exposure: effects of a methyl-supplemented diet

Downing, Chris; Johnson, Thomas E.; Larson, Colin; Leakey, Tatiana I.; Siegfried, Rachel N.; Rafferty, Tonya M.; Cooney, Craig A.

doi:10.1016/j.alcohol.2010.07.006

Cited by 93 publications

(93 citation statements)

References 46 publications

(59 reference statements)

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“…Fetal alcohol exposure also induced locus-specific alterations, including the insulin growth factor-II (IGF-II) locus. 44 Many of these alterations are correlated to changes in expression of genes that may contribute, in part, to the reported FASD phenotypes. 42 Although these studies suggest that alcohol exposure may induce the postnatal phenotypes through epigenetic remodeling, proof remains to be fully ascertained.…”

Section: -16mentioning

confidence: 99%

Back to the future: transgenerational transmission of xenobiotic-induced epigenetic remodeling

et al. 2015

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Section: -16mentioning

confidence: 99%

Back to the future: transgenerational transmission of xenobiotic-induced epigenetic remodeling

et al. 2015

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“…Hypermethylation of the MeCP2 promoter due to due to maternal (during pregnancy) alcohol use Mice Maternal alcohol exposure in early gestation [120,272] Decreased embryonic IGF2 promoter methylation and IGF 2 expression…”

Section: Hypomethylation Of the Pancreatic Il13ra2 Genementioning

confidence: 99%

“…Lower fasting serum triglyceride Rat Maternal Iron restriction for 4 weeks prior to and during pregnancy (7.5 mg kg −1 against the normal 50 mg kg −1 ) [134] Gestation day 13 male rat embryo showed significant upregulation of 979 genes and downregulation of 1545 genes involved in processes associated with the initiation of mitosis, BAD-mediated apoptosis, the assembly of RNA polymerase II preinitiation complexes and WNT signaling Upregulation of 7 proteins and downregulation of 10 proteins involved in cell proliferation, protein transport and folding, cytoskeletal remodeling and the proteasome complex Mice Maternal alcohol on gestational day 9 of pregnancy (5.8 g kg −1 ethanol) with or without methyl supplementation (15 g Choline, 15 g Betaine, 15 mg Folic Acid, 1.5 mg Vitamin B12, 7.5 g l-methionine, 150 mg Zinc) prior to, and during pregnancy and lactation [120] Methyl supplementation attenuated alcohol induced decreases in embryonic IGF2 promoter methylation and IGF 2 expression, and decreased mortality, and digit and vertebral malformations Zinc Rat Maternal zinc restriction 2 weeks before and during pregnancy (10 mg kg −1 diet against the normal 35 mg kg −1 ) [132] Lower offspring weight at birth, weaning and 6 months of age www.global-challenges.com Table 3. Continued.…”

Section: Upregulation Of Dnmt1 and Downregulation Of Dnmt3a And Dnmt3mentioning

confidence: 99%

“…[264] Prenatal exposure to alcohol is demonstrated to induce extensive DNA methylation changes in human [265][266][267] and rodent offsprings ( Table 2). [110,112,114,120,128,[268][269][270][271][272] These effects are possibly transmitted via methylation of the paternal germ line, [273] although alcohol-induced placental epigenetic changes suggest the involvement of the female germ line. [264] The rising harmful use of alcohol, [274] just as tobacco use, [275] imposes a huge public health burden, and may have contributed in shaping the history of some NCCDs in recent years.…”

Section: Smoking Alcohol Pollutants and Other Environmental Chemicalsmentioning

confidence: 99%

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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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“…Altered DNA methylation in offspring following adverse prenatal environmental conditions is not unique to the A vy allele, with changes to DNA methylation also reported at other genomic loci in both humans and experimental animal models following various prenatal exposures (Tobi et al, 2009;Kaminen-Ahola et al, 2010b;Downing et al, 2011;Bekdash et al, 2013;Laufer et al, 2013;Kile et al, 2014;Tobi et al, 2014;Amarasekera et al, 2014). Maternal tobacco smoking throughout pregnancy has been extensively associated with changes to DNA methylation in the blood of children (Joubert et al, 2012;Breton et al, 2014;Kupers et al, 2015;Lee et al, 2015;Joubert et al, 2016;Ladd-Acosta et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Yamada¹

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The in utero environment is a critical determinant of the immediate and future health of the developing fetus. In Australia, two of the most commonly used drugs during pregnancy are alcohol and nicotine. Prolonged periods of gestational exposure to alcohol and nicotine, separately, have been associated with a range of adverse outcomes in the offspring, in both humans and experimental animal models. The consequences of ethanol and nicotine exposure restricted to early gestation on resultant offspring are poorly characterised, and few animal models exist to build greater understanding. Moreover, the immediate molecular changes associated with exposures to ethanol and/or nicotine restricted to early gestation has yet to be described.This thesis utilised mouse models of early gestational ethanol and/or nicotine exposure to explore the impact of each of these exposures on offspring growth, as well as their associated transcriptional and epigenetic changes. In each model, pregnant C57BL/6 dams were provided with ad libitum access to solutions of 10% ethanol and/or 100 µg/ml nicotine from fertilisation (0.5 dpc) to midgestation (8.5 dpc). The exposure window utilised in each of the models is developmentally equivalent to the first three to four weeks of a human pregnancy.Previously, our laboratory identified reduced growth, microcephaly, and gene expression changes in the liver and hippocampus of the postnatal offspring of the model of prenatal ethanol exposure utilised in this thesis. In contrast, at mid-gestation (9.5 dpc), there was no evidence of developmental delay (somite number), reduced growth (crown-rump length), or microcephaly.Further, a genome-wide gene expression microarray (targeting 30 855 genes) and a screen of the expression of 641 microRNAs, identified only one gene (Bcl11b) as differentially expressed in male 9.5 dpc whole embryos following the ethanol exposure. These data suggest that there is a delay between the ethanol exposure and the onset of adverse phenotypes -arguing that the embryo is somehow able to form a memory of the ethanol exposure. The absence of widespread transcriptional changes suggests that changes in embryonic mRNA and microRNA expression are unlikely to be major contributors to the memory of the exposure.A early gestational model of nicotine exposure was newly established in this thesis. This nicotine exposure resulted in an average serum cotinine (metabolite of nicotine) concentration similar to that reported in humans who smoke 10 to 15 cigarettes per day. This exposure was sufficient to induce a reduction in body size both at mid-gestation and postnatally, but not at late gestation. Furthermore, the increased expression of Zscan10 in the whole male 9.5 dpc embryo was identified and validated across multiple cohorts. Zscan10 encodes for a transcription factor expressed throughout development, with a proposed role in the regulation of progenitor cells. The increased expression of Zscan10 in the nicotine-exposed embryos was associated with a reduction in DNA methylation ...

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Subtle decreases in DNA methylation and gene expression at the mouse Igf2 locus following prenatal alcohol exposure: effects of a methyl-supplemented diet

Cited by 93 publications

References 46 publications

Back to the future: transgenerational transmission of xenobiotic-induced epigenetic remodeling

Back to the future: transgenerational transmission of xenobiotic-induced epigenetic remodeling

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

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

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