Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Yang, Kefeng; Cai, Wei; Xu, Jiao; Shi, Wen

doi:10.1530/jme-12-0046

Cited by 37 publications

(22 citation statements)

References 32 publications

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“…Together with others reporting liver-tissue-specific fetal metabolic programming [73,74,75], the results discussed here clearly demonstrate that epigenetic cues for metabolic disease risk are established in utero. These results further corroborate our previous reports on hyperinsulinemia and hyperlipidemia observed in rat offspring born to diabetic and/or HF-fed dams, particularly during pregnancy [11].…”

Section: Discussionsupporting

confidence: 84%

Prenatal Exposure to a Maternal High-Fat Diet Affects Histone Modification of Cardiometabolic Genes in Newborn Rats

et al. 2017

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Infants born to women with diabetes or obesity are exposed to excess circulating fuels during fetal heart development and are at higher risk of cardiac diseases. We have previously shown that late-gestation diabetes, especially in conjunction with a maternal high-fat (HF) diet, impairs cardiac functions in rat-offspring. This study investigated changes in genome-wide histone modifications in newborn hearts from rat-pups exposed to maternal diabetes and HF-diet. Chromatin-immunoprecipitation-sequencing revealed a differential peak distribution on gene promoters in exposed pups with respect to acetylation of lysines 9 and 14 and to trimethylation of lysines 4 and 27 in histone H3 (all, false discovery rate, FDR < 0.1). In the HF-diet exposed offspring, 54% of the annotated genes showed the gene-activating mark trimethylated lysine 4. Many of these genes (1) are associated with the “metabolic process” in general and particularly with “positive regulation of cholesterol biosynthesis” (FDR = 0.03); (2) overlap with 455 quantitative trait loci for blood pressure, body weight, serum cholesterol (all, FDR < 0.1); and (3) are linked to cardiac disease susceptibility/progression, based on disease ontology analyses and scientific literature. These results indicate that maternal HF-diet changes the cardiac histone signature in offspring suggesting a fuel-mediated epigenetic reprogramming of cardiac tissue in utero.

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Section: Discussionsupporting

confidence: 84%

Prenatal Exposure to a Maternal High-Fat Diet Affects Histone Modification of Cardiometabolic Genes in Newborn Rats

et al. 2017

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“…Previous studies have linked high fat diets to epigenetic alterations of inhibitory histone markers such as H3K9Me3 (32, 33). Focusing on genes related to LPS response, we found WD male breeders had significantly greater H3K9Me3 histone modifications associated with the TLR4 and LPS binding protein (LBP) loci compared to their LF counterparts (Figure 5a).…”

Section: Resultsmentioning

confidence: 99%

Parental Dietary Fat Intake Alters Offspring Microbiome and Immunity

Myles

Fontecilla

Janelsins

et al. 2013

The Journal of Immunology

151

172

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Mechanisms underlying modern increases in prevalence of human inflammatory diseases remain unclear. The hygiene hypothesis postulates that decreased microbial exposure has, in part, driven this immune dysregulation. However, dietary fatty acids also influence immunity, partially through modulation of responses to microbes. Prior reports have described the direct effects of high fat diets on the gut microbiome and inflammation, and some have additionally shown metabolic consequences for offspring. Our study sought to expand on these previous observations to identify the effects of parental diet on offspring immunity using mouse models to provide insights into challenging aspects of human health. To test the hypothesis that parental dietary fat consumption during gestation and lactation influences offspring immunity, we compared pups of mice fed either a Western diet fatty acid profile or a standard low fat diet. All pups were weaned onto the control diet to specifically test the effects of early developmental fat exposure on immune development. Pups from Western diet breeders were not obese or diabetic, but still had worse outcomes in models of infection, autoimmunity, and allergic sensitization. They had heightened colonic inflammatory responses, with increased circulating bacterial lipopolysaccharide (LPS) and muted systemic LPS responsiveness. These deleterious impacts of the Western diet were associated with alterations of the offspring gut microbiome. These results indicate that parental fat consumption can leave a “lard legacy” impacting offspring immunity and suggest inheritable microbiota may contribute to the modern patterns of human health and disease.

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“…Maternal pregravid obesity is also associated with reduced abundance of the repressive histone mark H3K27me3 and increased expression of Zfp423, a key regulator committing cells to adipogenic lineage within fetal adipose tissue in rodent models. Furthermore, altered expression of Wnt genes in livers of offspring born to dams on HFD show hyperacetylation of Histone H4 and H3K9 . Additionally, studies in Japanese macaques have demonstrated elevated acetylation of the histone marks H3K9, H3K14, and H3K18 in fetal hepatic tissue exposed to HFD in utero .…”

Section: Introductionmentioning

confidence: 99%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.

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Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats

Cited by 37 publications

References 32 publications

Prenatal Exposure to a Maternal High-Fat Diet Affects Histone Modification of Cardiometabolic Genes in Newborn Rats

Prenatal Exposure to a Maternal High-Fat Diet Affects Histone Modification of Cardiometabolic Genes in Newborn Rats

Parental Dietary Fat Intake Alters Offspring Microbiome and Immunity

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

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