DNA Methylation in Oocytes and Liver of Female Mice and Their Offspring: Effects of High-Fat-Diet–Induced Obesity

Ge, Zhao‐Jia; Luo, Shi‐Ming; Lin, Fei; Liang, Qiu‐Xia; Huang, Lin; Wei, Yanchang; Hou, Yi; Han, Zhiming; Schatten, Heide; Sun, Qing‐Yuan

doi:10.1289/ehp.1307047

Cited by 136 publications

(115 citation statements)

References 48 publications

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“…The effect of maternal obesity (induced by 12-week preconceptional high-fat diet) on DNA methylation of particular metabolism-related genes in oocytes was also shown in a recent study by Ge et al [52]. Previous studies have reported that not only obesity, but also periconceptional undernutrition causes significant changes in DNA methylation that are maintained in adult offspring [53].…”

Section: The Effect Of Maternal Body Condition On Offspringmentioning

confidence: 64%

The effect of maternal body condition on in vivo production of zygotes and behavior of delivered offspring in mice

et al. 2015

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Section: The Effect Of Maternal Body Condition On Offspringmentioning

confidence: 64%

The effect of maternal body condition on in vivo production of zygotes and behavior of delivered offspring in mice

et al. 2015

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“…Evidence derived from mouse models would suggest that obesity leads to slower growth and delayed maturation of the oocyte, epigenetic modifications, increased granulosa cell apoptosis, and mitochondrial dysfunction within the oocyte (92,327,380). Hence, maternal obesity may exert germ-line effects by affecting oocyte quality and the methylation of imprinted genes, and in the mouse model, this has led to altered methylation patterns within metabolism-related genes in the oocytes and the liver of the offspring of obese mice (72,118). From mouse studies it has been demonstrated that maternal obesity leads to a deterioration in blastocyst development compared with matched controls; this effect can be overcome by intervention (218).…”

Section: Obesitymentioning

confidence: 99%

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Hart

2016

Physiological Reviews

156

109

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Across the Western World there is an increasing trend to postpone childbearing. Consequently, the negative influence of age on oocyte quality may lead to a difficulty in conceiving for many couples. Furthermore, lifestyle factors may exacerbate a couple's difficulty in conceiving due mainly to the metabolic influence of obesity; however, the negative impacts of low peripheral body fat, excessive exercise, the increasing prevalence of sexually transmitted diseases, and smoking all have significant negative effects on fertility. Other factors that impede conception are the perceived increasing prevalence of the polycystic ovary syndrome, which is further exacerbated by obesity, and the presence of uterine fibroids and endometriosis (a progressive pelvic inflammatory disorder) which are more prevalent in older women. A tendency for an earlier sexual debut and to have more sexual partners has led to an increase in sexually transmitted diseases. In addition, there are several genetic influences that may limit the number of oocytes within the ovary; consequently, by postponing attempts at childbearing, a limitation of oocyte number may become evident, whereas in previous generations with earlier conception this potentially reduced reproductive life span did not manifest in infertility. Environmental influences on reproduction are under increasing scrutiny. Although firm evidence is lacking however, dioxin exposure may be linked to endometriosis, phthalate exposure may influence ovarian reserve, and bisphenol A may interfere with oocyte development and maturation. However, chemotherapy or radiotherapy is recognized to lead to ovarian damage and predispose the woman to ovarian failure.

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“…For example, maternal obesity is associated with numerous markers of reduced oocyte quality, including impaired maturation (17,35), increased lipid content (86,87), cellular lipotoxicity (87), alterations to mitochondria including ultrastructure (30), membrane potential (32), and mitochondrial DNA (mtDNA) content (32,88), as well as increased reactive oxygen species and depleted glutathione (indicative of oxidative stress) (32,52) and alterations to DNA methylation patterns of key metabolic and imprinting genes in oocytes (29), resulting from reduced DNA methyltransferase levels (28,29). In males, paternal obesity increases sperm oxidative stress and DNA damage (3,38,69,81) and alters sperm microRNA content (23,55), lipid content (20), protein composition (39,51,70,77), and active and repressive chromatin state (68) and global DNA hypomethylation (23).…”

mentioning

confidence: 99%

When two obese parents are worse than one! Impacts on embryo and fetal development

McPherson

Bell

Zander-Fox

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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McPherson NO, Bell VG, Zander-Fox DL, Fullston T, Wu LL, Robker RL, Lane M. When two obese parents are worse than one! Impacts on embryo and fetal development. Am J Physiol Endocrinol Metab 309: E568 -E581, 2015. First published July 21, 2015; doi:10.1152/ajpendo.00230.2015.-The prevalence of overweight and obesity in reproductive-age adults is increasing worldwide. While the effects of either paternal or maternal obesity on gamete health and subsequent fertility and pregnancy have been reported independently, the combination of having both parents overweight/ obese on fecundity and offspring health has received minimal attention. Using a 2 ϫ 2 study design in rodents we established the relative contributions of paternal and maternal obesity on fetal and embryo development and whether combined paternal and maternal obesity had an additive effect. Here, we show that parental obesity reduces fetal and placental weights without altering pregnancy establishment and is not dependent on an in utero exposure to a high-fat diet. Interestingly combined parental obesity seemed to accumulate both the negative influences of paternal and maternal obesity had alone on embryo and fetal health rather than an amplification, manifested as reduced embryo developmental competency, reduced blastocyst cell numbers, impaired mitochondrial function, and alterations to active and repressive embryonic chromatin marks, resulting in aberrant placental gene expression and reduced fetal liver mtDNA copy numbers. Further understanding both the maternal cytoplasmic and paternal genetic interactions during this early developmental time frame will be vital for understanding how developmental programming is regulated and for the proposition of interventions to mitigate their effects. blastocyst; oocyte; sperm; embryo; fertility; infertility; obesity THE PREVALENCE OF OVERWEIGHT and obesity in reproductive-age adults is increasing worldwide (62). For example, in America it is estimated that 70.9% of males and 61.9% of women are classified as overweight/obese (62). The comorbidities associated with obesity have been well defined; however, until recently the impact on pregnancy and fetal development has been less recognized. Although the effects of either paternal or maternal obesity on gamete health and subsequent fertility and pregnancy have been reported independently, the combination of having both parents overweight/obese on fecundity and offspring health has received minimal attention. This information is essential, as the percentage of couples of reproductive age with both partners overweight/ obese is increasing and is the predominant situation in many countries (62).To date, there have only been three studies that have assessed the combined effects of maternal and paternal obesity on pregnancy and fetal health, two in human-assisted reproductive technology (ART) cohorts and one using a rodent high-fat diet model (41,67,76). These studies found no effect of maternal and paternal obesity on pregnancy establishment (41, 67, 76); however, when ...

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DNA Methylation in Oocytes and Liver of Female Mice and Their Offspring: Effects of High-Fat-Diet–Induced Obesity

Cited by 136 publications

References 48 publications

The effect of maternal body condition on in vivo production of zygotes and behavior of delivered offspring in mice

The effect of maternal body condition on in vivo production of zygotes and behavior of delivered offspring in mice

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

When two obese parents are worse than one! Impacts on embryo and fetal development

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