Maternal low-protein diet causes epigenetic deregulation of HMGCR and CYP7α1 in the liver of weaning piglets

Cong, Rihua; Jia, Yimin; R, Li; Ni, Yingdong; Yang, Xia; Sun, Qinwei; Parvizi, Nahid; Zhao, Ruqian

doi:10.1016/j.jnutbio.2011.11.007

Cited by 53 publications

(36 citation statements)

References 52 publications

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“…A previous study reported that food restriction during pregnancy enhances hepatic HMGCR mRNA expression in adult offspring and that hypomethylation and hyperacetylation occur in the HMGCR gene promoter [13]. This finding suggests that the alterations in hepatic cholesterol metabolism with epigenetic modifications result in an abnormal blood cholesterol levels.…”

Section: Discussionmentioning

confidence: 94%

“…An adverse prenatal environment probably causes serum cholesterol disorders of offspring by influencing hepatic cholesterol metabolism [11]. It was found that serum TCH was increased in IUGR offspring rats [14], expression levels of hepatic HMGCR and CYP7A1 were increased, and epigenetic modification changes in hypomethylation and hyperacetylation were found [13]. Also, mRNA expression of LDLR, which help carry cholesterol back to the liver from the peripheral circulation, was decreased [33].…”

Section: Discussionmentioning

confidence: 99%

“…Because the liver is the largest cholesterol metabolic organ, hepatic cholesterol metabolic disorders can directly cause blood cholesterol disorders and are involved in many types of cerebrovascular diseases. It has been reported that increased blood cholesterol level that both occurs after the birth of offspring, and is caused by an adverse prenatal environment may be related to the changes in hepatic cholesterol metabolism [10, 13, 14]. Therefore, the changes in hepatic cholesterol metabolism in IUGR offspring are worthy of great attention [10, 15].…”

Section: Introductionmentioning

confidence: 99%

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Effects and Interactions of Prenatal Ethanol Exposure, a Post-Weaning High-Fat Diet and Gender on Adult Hypercholesterolemia Occurrence in Offspring Rats

Qi¹,

Luo²,

Hu³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Prenatal ethanol exposure (PEE) could induce intrauterine programming of hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolism, resulting in intrauterine growth retardation and susceptibility to adult hypercholesterolemia in offspring. This study aimed to analyse the effects and interactions of PEE, a post-weaning high-fat diet (HFD) and gender on the occurrence of adult hypercholesterolemia in offspring rats. Methods: Wistar female rats were treated with ethanol (4 g/kg.d) at gestational days 11-20. The offspring were given a normal diet or HFD after weaning, and the blood cholesterol metabolism phenotype and expression of hepatic cholesterol metabolism related genes were detected in 24-week-old offspring. Furthermore, the interactions among PEE, HFD, and gender on hypercholesterolemia occurrence were analysed. Results: PEE increased the serum total cholesterol (TCH) and low-density lipoprotein-cholesterol (LDL-C) levels and decreased the serum high-density lipoprotein-cholesterol (HDL-C) level in adult offspring rats; the changes in female offspring were greater than those in males. At the same time, the mRNA expression levels of hepatic cholesterol metabolic enzymes (apolipoprotein B (ApoB) and 7α-hydroxylase (CYP7A1))—were increased, while the mRNA expression levels of the scavenger receptor B1 (SR-B1) and LDL receptor (LDLR) were decreased. Furthermore, a three-way ANOVA showed there were interactions among PEE, post-weaning HFD and gender. For PEE offspring, a post-weaning HFD aggravated the elevated hepatic ApoB and CYP7A1 expression and reduced SR-B1 and LDLR expression; the changes in hepatic SR-B1 and CYP7A1 expression were greater in female HFD rats than in males. Conclusion: Our findings suggest that a post-weaning HFD could aggravate offspring hypercholesterolemia caused by PEE and that this mechanism might be associated with hepatic cholesterol metabolic disorders that are aggravated by a post-weaning HFD; hepatic cholesterol metabolism was more sensitive to neuroendocrine metabolic alterations by PEE and a post-weaning HFD in the female offspring than in the male offspring.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects and Interactions of Prenatal Ethanol Exposure, a Post-Weaning High-Fat Diet and Gender on Adult Hypercholesterolemia Occurrence in Offspring Rats

Qi¹,

Luo²,

Hu³

et al. 2017

Cell Physiol Biochem

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show abstract

“…MeDIP analysis was performed as previously described [27], with some modifications. High-quality liver genomic DNA was isolated and sonicated to produce small fragments of approximately 200e500 bp.…”

Section: Methylated Dna Immunoprecipitation (Medip) Analysismentioning

confidence: 99%

α-Lipoic acid attenuates LPS-induced liver injury by improving mitochondrial function in association with GR mitochondrial DNA occupancy

et al. 2015

Self Cite

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“…In a potentially unrelated mechanism, low-protein diets in porcine models during the gestational-lactation period were shown to alter offspring body and organ weight [36]. These phenotypic changes were associated with serum and liver cholesterol levels as well as hepatic upregulation of genes involved in cholesterol biosynthesis and metabolism (3-hydroxy-3-methylglutaryl-CoA, HMGCR and cholesterol-7-alpha-hydroxylase, CYP7a1).…”

Section: Direct and Indirect Effectsmentioning

confidence: 99%

Maternal Nutrition and Epigenetic Perturbation: Modeling Trends to Translation

Oakes

Ideraabdullah

2013

Curr Pediatr Rep

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Maternal nutrition plays an essential role in offspring health and development. Critical stages include: (1) preconception, affecting oocyte development and uterine environment preparation; (2) gestation, affecting uterine environment and placental nutrient transfer and (3) postnatal, through lactation. It remains debatable which stage is most important, but arguably, the most complex cellular events occur during gestation. During this time, embryo development requires a well orchestrated and tightly regulated cascade of genetic, molecular and biochemical events. Among these are epigenetic events necessary for gene expression regulation. These produce heritable yet often reversible states established based on transcriptional needs of the cell. A growing body of research highlights the role of maternal nutrition in determining epigenetic states important for pre-and postnatal development. Here, we discuss recent findings addressing epigenetic response to nutrition with relevance to developmental origins of phenotypic outcome.

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Maternal low-protein diet causes epigenetic deregulation of HMGCR and CYP7α1 in the liver of weaning piglets

Cited by 53 publications

References 52 publications

Effects and Interactions of Prenatal Ethanol Exposure, a Post-Weaning High-Fat Diet and Gender on Adult Hypercholesterolemia Occurrence in Offspring Rats

Effects and Interactions of Prenatal Ethanol Exposure, a Post-Weaning High-Fat Diet and Gender on Adult Hypercholesterolemia Occurrence in Offspring Rats

α-Lipoic acid attenuates LPS-induced liver injury by improving mitochondrial function in association with GR mitochondrial DNA occupancy

Maternal Nutrition and Epigenetic Perturbation: Modeling Trends to Translation

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