The effect of maternal consumption of high-fat diet on ovarian development in offspring

Wei, Wenyan; Qin, Feng; Gao, Junjie; Chang, Junlei; Pan, Xujing; Jiang, Xin; Che, Lianqiang; Zhuo, Yong; Xu, Shengyu

doi:10.1016/j.anireprosci.2023.107294

Cited by 12 publications

(3 citation statements)

References 88 publications

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“…Nevertheless, the positive correlation between cholesterol and triglycerides and the number of apoptotic follicles was consistent with previous data highlighting that cholesterol abundance promotes reactive oxygen species and exacerbates apoptotic cell death in the ovarian cell [81]. More recent studies have shown that a high-fat maternal diet affects the expression of genes related to follicle growth in offspring, such as AAT (α1-antitrypsin), AFP (α-fetoprotein) and GDF-9 (growth differentiation-9), reducing the number of follicles and altering the development of follicles [80]. Additionally, a high-fat maternal diet also affects ovarian health by inducing ovarian oxidative stress and cellular apoptosis, which collectively can impair the reproductive potential of female offspring.…”

Section: Gonadal Phenotypesupporting

confidence: 92%

“…These data are consistent with previous studies related to the administration of a high-fat diet. Indeed, a high-fat diet was shown to reduce the ovarian surface area and to increase ovarian atresia in mice, rats and rabbits, impairing follicular reserve [36,79,80]. The higher number of atretic follicles suggests a possible increase in apoptotic mechanisms during folliculogenesis.…”

Section: Gonadal Phenotypementioning

confidence: 99%

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The Effect of Maternal Exposure to a Diet High in Fats and Cholesterol on the Placental Function and Phenotype of the Offspring in a Rabbit Model: A Summary Review of About 15 Years of Research

Rousseau-Ralliard,

Chavatte-Palmer,

Couturier-Tarrade

2023

IJMS

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The rates of obesity and being overweight are increasing all around the world, especially among women of childbearing age, in part due to overconsumption of lipids. The aim of this summary review was to present the cellular and molecular effects of a hyperlipidic high-cholesterol (H) diet on the maternal and offspring phenotype at the early embryonic, neonatal, weaning and adult stages while considering the effects of sex and to identify the window(s) of vulnerability linked to this exposure in a rabbit model. Before breeding, the H diet induced dyslipidemia and aortic atherosclerosis lesions and increased the number of atretic follicles. In the offspring, the H diet disrupted the embryonic phenotype and induced fetal hypotrophy associated with sex-specific disturbances of the feto-placental unit. In adulthood, the offspring of the H dams were heavier and hyperphagic and had increased blood pressure associated with disturbed gonadal development in both sexes. Vulnerability windows were explored via embryo transfers. The maternal gestational diet was shown to play a key role in the feto-placental phenotype, and preconception programming was unquestionably also observed. These two periods could represent windows of intervention in the context of obesity or being overweight to limit fetal and placental consequences.

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Section: Gonadal Phenotypesupporting

confidence: 92%

Section: Gonadal Phenotypementioning

confidence: 99%

The Effect of Maternal Exposure to a Diet High in Fats and Cholesterol on the Placental Function and Phenotype of the Offspring in a Rabbit Model: A Summary Review of About 15 Years of Research

Rousseau-Ralliard,

Chavatte-Palmer,

Couturier-Tarrade

2023

IJMS

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“…Moreover, children born to obese mothers have increased risk of developing metabolic syndrome, including obesity and diabetes [ 3 ], and are thus more prone to the development of metabolic diseases later in life [ 4 – 7 ]. A few studies in diet-induced obese mouse models suggested that maternal obesity increases the risk of reproductive disorders in the offspring as well [ 8 – 10 ]. Since children mostly follow the same lifestyle and dietary habits of their parents [ 11 ], some of the reported effects of maternal obesity on offspring health and fertility can be, at least in part, due to direct effects of consuming obesogenic (OB) diets after ablactation.…”

Section: Introductionmentioning

confidence: 99%

The impact of offspring and maternal obesogenic diets on adult offspring oocyte mitochondrial morphology in primordial and preantral follicles

Xhonneux,

Marei,

Meulders

et al. 2024

PLoS ONE

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Diet-induced obesity reduces oocyte quality mainly by impacting oocyte mitochondrial functions. Moreover, maternal obesity is associated with mitochondrial dysfunction in oocytes of their adult offspring. However, these effects were reported only in fully grown oocytes, mainly in the form of abnormal mitochondrial ultrastructure. It is unknown if obesogenic (OB) diets or maternal obesity already impact the primordial and preantral follicles. Considering the long duration and dynamics of folliculogenesis, determining the stage at which oocytes are affected and the extent of the damage is crucial for optimal reproductive management of obese patients and their daughters. Potential interaction between maternal and offspring diet effects are also not described, yet pivotal in our contemporary society. Therefore, here we examined the impact of OB diets on oocyte mitochondrial ultrastructure in primordial and activated preantral follicles in offspring from diet-induced obese or lean mothers. We used an outbred Swiss mouse model to increase the pathophysiological relevance to humans. Female mice were fed control or OB diets for 7 weeks, then mated with control males. Their female offspring were fed control or OB diets after weaning for 7 weeks (2-by-2 factorial design). Adult offspring ovarian sections were examined using transmission electron microscopy. We characterised and classified unique features of oocyte mitochondrial ultrastructure in the preantral follicles. An increase in mitochondrial matrix density was the most predominant change during follicle activation in secondary follicles, a feature that is linked with a higher mitochondrial activity. Maternal obesity increased mitochondrial density already in the primordial follicles suggesting an earlier increase in bioenergetic capacity. Maternal obesity did not induce abberant ultrastructure (abnormalities and defects) in primordial or preantral follicles. In contrast, offspring OB diet increased mitochondrial abnormalities in the primordial follicles. Further investigation of the consequences of these changes on oocyte metabolic regulation and stress levels during folliculogenesis is needed.

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Beyond defence: Immune architects of ovarian health and disease

Bazzano,

Köninger,

Solano

2024

Semin Immunopathol

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Throughout the individual’s reproductive period of life the ovary undergoes continues changes, including cyclic processes of cell death, tissue regeneration, proliferation, and vascularization. Tissue-resident leucocytes particularly macrophages, play a crucial role in shaping ovarian function and maintaining homeostasis. Macrophages crucially promote angiogenesis in the follicles and corpora lutea, thereby supporting steroidogenesis. Recent research on macrophage origins and early tissue seeding has unveiled significant insights into their role in early organogenesis, e.g. in the testis. Here, we review evidence about the prenatal ovarian seeding of leucocytes, primarily macrophages with angiogenic profiles, and its connection to gametogenesis. In the prenatal ovary, germ cells proliferate, form cysts, and undergo changes that, following waves of apoptosis, give rice to the oocytes contained in primordial follicles. These follicles constitute the ovarian reserve that lasts throughout the female’s reproductive life. Simultaneously, yolk-sac-derived primitive macrophages colonizing the early ovary are gradually replaced or outnumbered by monocyte-derived fetal macrophages. However, the cues indicating how macrophage colonization and follicle assembly are related are elusive. Macrophages may contribute to organogenesis by promoting early vasculogenesis. Whether macrophages contribute to ovarian lymphangiogenesis or innervation is still unknown. Ovarian organogenesis and gametogenesis are vulnerable to prenatal insults, potentially programming dysfunction in later life, as observed in polycystic ovary syndrome. Experimental and, more sparsely, epidemiological evidence suggest that adverse stimuli during pregnancy can program defective folliculogenesis or a diminished follicle reserve in the offspring. While the ovary is highly sensitive to inflammation, the involvement of local immune responses in programming ovarian health and disease remains to be thoroughly investigated.

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The effect of maternal consumption of high-fat diet on ovarian development in offspring

Cited by 12 publications

References 88 publications

The Effect of Maternal Exposure to a Diet High in Fats and Cholesterol on the Placental Function and Phenotype of the Offspring in a Rabbit Model: A Summary Review of About 15 Years of Research

The Effect of Maternal Exposure to a Diet High in Fats and Cholesterol on the Placental Function and Phenotype of the Offspring in a Rabbit Model: A Summary Review of About 15 Years of Research

The impact of offspring and maternal obesogenic diets on adult offspring oocyte mitochondrial morphology in primordial and preantral follicles

Beyond defence: Immune architects of ovarian health and disease

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