The nonalcoholic fatty liver disease-like phenotype and lowered serum VLDL are associated with decreased expression and DNA hypermethylation of hepatic ApoB in male offspring of ApoE deficient mothers fed a with Western diet

Chen, Hao Ming; Chen, Yi Zhen; Wang, Chih Hong; Lin, Fei-Jan

doi:10.1016/j.jnutbio.2019.108319

Cited by 17 publications

(14 citation statements)

References 60 publications

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“…Studies from our laboratory found that in the rat prostate gland [ 58 ], neonatal exposure to estradiol/BPA alters the transcriptional program of factors involved in DNA methylation (DNMT3A/B and MBD2/4) and hypomethylation of the promoter of nucleosome binding protein-1 (NSBP1), an early and permanent epigenetic mark of neonatal exposure to estradiol/bisphenol A that persists throughout life. Additionally, maternal high-fat diets in mice have been found to be associated with altered gene expression, chromatin marks, and DNA methylation changes [ 82 , 83 , 84 ] in male and female offspring. However, in our present study, we did not observe any consistent changes in transcripts for the DNA methyl transferases, or for the methyl-CpG-binding domain proteins MBD1, MBD2 , or MBD4 between the various groups in the F1- and F3-generation offspring.…”

Section: Discussionmentioning

confidence: 99%

Three-Generation Study of Male Rats Gestationally Exposed to High Butterfat and Bisphenol A: Impaired Spermatogenesis, Penetrance with Reduced Severity

Rao

Ouyang

et al. 2021

Nutrients

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Gestational high butterfat (HFB) and/or endocrine disruptor exposure was previously found to disrupt spermatogenesis in adulthood. This study addresses the data gap in our knowledge regarding transgenerational transmission of the disruptive interaction between a high-fat diet and endocrine disruptor bisphenol A (BPA). F0 generation Sprague-Dawley rats were fed diets containing butterfat (10 kcal%) and high in butterfat (39 kcal%, HFB) with or without BPA (25 µg/kg body weight/day) during mating and pregnancy. Gestationally exposed F1-generation offspring from different litters were mated to produce F2 offspring, and similarly, F2-generation animals produced F3-generation offspring. One group of F3 male offspring was administered either testosterone plus estradiol-17β (T + E2) or sham via capsule implants from postnatal days 70 to 210. Another group was naturally aged to 18 months. Combination diets of HFB + BPA in F0 dams, but not single exposure to either, disrupted spermatogenesis in F3-generation adult males in both the T + E2-implanted group and the naturally aged group. CYP19A1 localization to the acrosome and estrogen receptor beta (ERbeta) localization to the nucleus were associated with impaired spermatogenesis. Finally, expression of methyl-CpG-binding domain-3 (MBD3) was consistently decreased in the HFB and HFB + BPA exposed F1 and F3 testes, suggesting an epigenetic component to this inheritance. However, the severe atrophy within testes present in F1 males was absent in F3 males. In conclusion, the HFB + BPA group demonstrated transgenerational inheritance of the impaired spermatogenesis phenotype, but severity was reduced in the F3 generation.

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Section: Discussionmentioning

confidence: 99%

Three-Generation Study of Male Rats Gestationally Exposed to High Butterfat and Bisphenol A: Impaired Spermatogenesis, Penetrance with Reduced Severity

Rao

Ouyang

et al. 2021

Nutrients

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“…Diet plays a pivotal role in DNA methylation through several ways, including regulating the activity of enzymes associated with the one-carbon cycle and providing SAM as methyl donors. 169 Recently, Chen et al 170 revealed that maternal consumption of a high-fat or high-cholesterol western diet can induce the pathogenesis of NAFLD in male offspring by modulating the expression of the apolipoprotein B (ApoB) gene. Based on DNA methylation analysis, they found that the ApoB gene promoter region presents increased methylation of CpG dinucleotides.…”

Section: Epigenetic Regulatory Mechanisms In Metabolic Diseasesmentioning

confidence: 99%

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Lin

et al. 2023

Sig Transduct Target Ther

134

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Epigenetics regulates gene expression and has been confirmed to play a critical role in a variety of metabolic diseases, such as diabetes, obesity, non-alcoholic fatty liver disease (NAFLD), osteoporosis, gout, hyperthyroidism, hypothyroidism and others. The term ‘epigenetics’ was firstly proposed in 1942 and with the development of technologies, the exploration of epigenetics has made great progresses. There are four main epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodelling, and noncoding RNA (ncRNA), which exert different effects on metabolic diseases. Genetic and non-genetic factors, including ageing, diet, and exercise, interact with epigenetics and jointly affect the formation of a phenotype. Understanding epigenetics could be applied to diagnosing and treating metabolic diseases in the clinic, including epigenetic biomarkers, epigenetic drugs, and epigenetic editing. In this review, we introduce the brief history of epigenetics as well as the milestone events since the proposal of the term ‘epigenetics’. Moreover, we summarise the research methods of epigenetics and introduce four main general mechanisms of epigenetic modulation. Furthermore, we summarise epigenetic mechanisms in metabolic diseases and introduce the interaction between epigenetics and genetic or non-genetic factors. Finally, we introduce the clinical trials and applications of epigenetics in metabolic diseases.

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“…In a related study by Chen et al., maternal high fat/cholesterol diet exacerbated the establishment of NAFLD in male offspring by low hepatic ApoB gene expression and hypermethylation of CpG dinucleotides in the promoter region of ApoB gene compared to male offspring born to chow fed mice. Increased methylation of ApoB gene that is essential for VLDL assembly results in low expression of Apo-B in livers contributing to altered lipid profile and lipid transport from liver [ 170 ]. Deregulated Nuclear factor erythroid related factor2 (NRF2) signaling cascades play an important role in liver diseases.…”

Section: Lifestyle Variables As Dna Methylations Modifiersmentioning

confidence: 99%

Deciphering the role of aberrant DNA methylation in NAFLD and NASH

Vachher¹,

Bansal²,

Kumar

et al. 2022

Heliyon

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The nonalcoholic fatty liver disease-like phenotype and lowered serum VLDL are associated with decreased expression and DNA hypermethylation of hepatic ApoB in male offspring of ApoE deficient mothers fed a with Western diet

Cited by 17 publications

References 60 publications

Three-Generation Study of Male Rats Gestationally Exposed to High Butterfat and Bisphenol A: Impaired Spermatogenesis, Penetrance with Reduced Severity

Three-Generation Study of Male Rats Gestationally Exposed to High Butterfat and Bisphenol A: Impaired Spermatogenesis, Penetrance with Reduced Severity

Epigenetic regulation in metabolic diseases: mechanisms and advances in clinical study

Deciphering the role of aberrant DNA methylation in NAFLD and NASH

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