The fetal programming effect of prenatal smoking on<i>Igf1r</i>and<i>Igf1</i>methylation is organ- and sex-specific

Meyer, Karolin F; Verkaik-Schakel, Rikst Nynke; Timens, Wim; Kobzik, Lester; Plösch, Torsten; Hylkema, Machteld N.

doi:10.1080/15592294.2017.1403691

Cited by 18 publications

(22 citation statements)

References 42 publications

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“…This beneficial effect of NAC was not found in livers of male offspring, suggesting a tissue specific effect of NAC. A tissue-specific response, with a distinct DNA methylation pattern, was observed in several models of prenatal exposure to stressors [17][18][19]. Uncovering the DNA methylome in muscle, liver and pancreatic islets might shed light on the tissue-specific outcomes of prenatal NAC administration.…”

Section: Discussionmentioning

confidence: 99%

Maternal N-Acetyl Cysteine Intake Improved Glucose Tolerance in Obese Mice Offspring

Michlin

Argaev-Frenkel

Weinstein-Fudim³

et al. 2020

IJMS

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Exposure to certain environmental factors during the early stages of development was found to affect health in adulthood. Among other environmental factors, oxidative stress has been suggested to be involved in fetal programming, leading to elevated risk for metabolic disorders, including type 2 diabetes; however, the possibility that antioxidant consumption during early life may affect the development of diabetes has scarcely been studied. The aim of this study was to investigate the effects of N-acetyl-l-cysteine (NAC) given during pregnancy and lactation on the susceptibility of offspring to develop glucose intolerance at adulthood. C57bl6/J mice were given NAC during pregnancy and lactation. High fat diet (HFD) was given to offspring at an age of 6 weeks for an additional 9 weeks, till the end of the study. Isolated islets of NAC-treated offspring (6 weeks old, before HFD feeding) had an increased efficacy of glucose-stimulated insulin secretion and a higher resistance to oxidative damage. Following HFD feeding, glucose tolerance and insulin sensitivity of NAC-treated offspring were improved. In addition, islet diameter was lower in male offspring of NAC-treated mice compared to their HFD-fed littermates. NAC consumption during early life improves glucose tolerance in adulthood in mice.

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Section: Discussionmentioning

confidence: 99%

Maternal N-Acetyl Cysteine Intake Improved Glucose Tolerance in Obese Mice Offspring

Michlin

Argaev-Frenkel

Weinstein-Fudim³

et al. 2020

IJMS

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“…Cigarette smoking has adverse effects on health and is associated with changes in epigenetic marks. Prenatal smoke exposure affects DNA methylation in blood cells from children of smoking mothers [ 185 , 186 ]. Smoking may induce DNA methylation alterations in cells of both the innate and adaptive immune systems [ 187 ].…”

Section: Epigenetics and Agingmentioning

confidence: 99%

Polyamine Metabolism and Gene Methylation in Conjunction with One-Carbon Metabolism

Soda

2018

IJMS

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Recent investigations have revealed that changes in DNA methylation status play an important role in aging-associated pathologies and lifespan. The methylation of DNA is regulated by DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) in the presence of S-adenosylmethionine (SAM), which serves as a methyl group donor. Increased availability of SAM enhances DNMT activity, while its metabolites, S-adenosyl-l-homocysteine (SAH) and decarboxylated S-adenosylmethionine (dcSAM), act to inhibit DNMT activity. SAH, which is converted from SAM by adding a methyl group to cytosine residues in DNA, is an intermediate precursor of homocysteine. dcSAM, converted from SAM by the enzymatic activity of adenosylmethionine decarboxylase, provides an aminopropyl group to synthesize the polyamines spermine and spermidine. Increased homocysteine levels are a significant risk factor for the development of a wide range of conditions, including cardiovascular diseases. However, successful homocysteine-lowering treatment by vitamins (B6, B12, and folate) failed to improve these conditions. Long-term increased polyamine intake elevated blood spermine levels and inhibited aging-associated pathologies in mice and humans. Spermine reversed changes (increased dcSAM, decreased DNMT activity, aberrant DNA methylation, and proinflammatory status) induced by the inhibition of ornithine decarboxylase. The relation between polyamine metabolism, one-carbon metabolism, DNA methylation, and the biological mechanism of spermine-induced lifespan extension is discussed.

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“…This was related to sex-dependent differences in promoter methylation of Igf1r . This was recently confirmed in a second study using a prenatal smoke model in C57Bl/6 mice, which also showed that Igfr1 CpG methylation was organ- and sex-specific 64 . The difference to our study could be due to the different time point of analysis as the observed increase in Igf1 levels in our study was only found at E18.5, but not at PND 21 and we did not investigate d30.…”

Section: Discussionmentioning

confidence: 55%

Intrauterine smoke exposure deregulates lung function, pulmonary transcriptomes, and in particular insulin-like growth factor (IGF)-1 in a sex-specific manner

Dehmel

Nathan

Bartel

et al. 2018

Sci Rep

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Prenatal exposure to tobacco smoke is a significant risk-factor for airway disease development. Furthermore, the high prevalence of pregnant smoking women requires the establishment of strategies for offspring lung protection. Therefore, we here aimed to understand the molecular mechanism of how prenatal smoke exposure affects fetal lung development. We used a mouse model recapitulating clinical findings of prenatally exposed children, where pregnant mice were exposed to smoke until c-section or spontaneous delivery, and offspring weight development and lung function was monitored. Additionally, we investigated pulmonary transcriptome changes in fetal lungs (GD18.5) by mRNA/miRNA arrays, network analyses and qPCR. The results demonstrated that prenatally exposed mice showed intrauterine and postnatal growth retardation, and impaired lung function. 1340 genes and 133 miRNAs were found to be significantly dysregulated by in utero smoke exposure, and we identified Insulin-like growth factor 1 (Igf1) as a top hierarchical node in a network analysis. Moreover, Igf1 mRNA was increased in female murine offspring and in prenatally exposed children. These findings suggest that prenatal smoking is associated with a dysregulation of several genes, including Igf1 in a sex-specific manner. Thus, our results could represent a novel link between smoke exposure, abberant lung development and impaired lung function.

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The fetal programming effect of prenatal smoking onIgf1randIgf1methylation is organ- and sex-specific

Cited by 18 publications

References 42 publications

Maternal N-Acetyl Cysteine Intake Improved Glucose Tolerance in Obese Mice Offspring

Maternal N-Acetyl Cysteine Intake Improved Glucose Tolerance in Obese Mice Offspring

Polyamine Metabolism and Gene Methylation in Conjunction with One-Carbon Metabolism

Intrauterine smoke exposure deregulates lung function, pulmonary transcriptomes, and in particular insulin-like growth factor (IGF)-1 in a sex-specific manner

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