Obesity accelerates ovarian follicle development and follicle loss in rats

Wang, Na; Luo, Lili; Xu, Jianhui; Xu, Ming-Yan XuM.-Y; Zhang, Xingmei; Zhou, Xiaoling; Liu, Wei-Juan; Fu, Yucai

doi:10.1016/j.metabol.2013.09.001

Cited by 130 publications

(101 citation statements)

References 56 publications

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“…Despite the difference in the biological model, these results are consistent with previous studies. Wang et al 44 reported that high-fat-induced obesity stimulates the activation of Po follicles and promotes the development and maturity of ovarian follicles. These authors also found that rats fed with high fat display a lower number of Po follicles and a greater number of developing follicles and corpora lutea in parallel with a greater number of atretic follicles.…”

Section: Discussionmentioning

confidence: 99%

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Maternal Overweight Disrupts the Sexual Maturation of the Offspring

et al. 2017

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The aims of the present work were to study the effect of maternal overweight and obesity on the ovarian reserve, follicular development, and ovulation of the offspring and to assess whether this maternal condition alters oocyte integrity. To this end, female offspring from rats fed standard (OSD) or cafeteria (OCD) diet were used. Body weight, vaginal opening, and estrous cycle were recorded and ovaries were obtained on the day of the second estrus. In addition, ovarian weight, ovulation rate (measured by the number of oocytes within oviducts), follicular development (determined by histology), and oocyte integrity were examined. The OCD were divided into 2 groups: offspring from rats with 17% and 28% of overweight (OCD17 and OCD28, respectively). Both OCD groups showed higher body weight, but OCD28 also exhibited early vaginal opening and higher ovarian weight and glycemia at euthanasia compared with OSD. Both OCD17 and OCD28 had lower number of primordial and primary follicles, and only OCD28 exhibited lower number of antral follicles, all compared with OSD rats. In addition, both OCD17 and OCD28 had higher ovulation rate than controls, and OCD28 had lower number of healthy oocytes, which, in turn, exhibited morphological alterations such as larger perivitelline space and zona pellucida than those of control animals. These results suggest that maternal overweight may severely affect the reproductive ability of the offspring, likely as a result of altering the organogenesis.

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Section: Discussionmentioning

confidence: 99%

“…The mechanism involved in these effects still needs to be elucidated, though it is probable that the reduction in viability percentage is due to a greater apoptosis rate, as observed by other authors. 44,[54][55][56][57] However, more studies regarding this issue are in progress in our laboratory.…”

Section: Discussionmentioning

confidence: 99%

Maternal Overweight Disrupts the Sexual Maturation of the Offspring

et al. 2017

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“…In rat ovaries caloric restriction and rapamycin seem to inhibit the transition from primordial to developing follicles and preserve the follicle pool reserve through a fine-tuning of SIRT1 signalling (30,31). By contrast in ovaries from high fat diet, down-regulation of SIRT1 signalling was associated with accelerated ovarian development and follicle loss (32). In mammalian GCs, the oocyte companion cells the role of sirtuins has been so far poorly investigated.…”

Section: Sirtuins Expression and Functions In The Mammalian Folliclementioning

confidence: 99%

Follicle aging: a question of stress?

Tatone¹

2015

CCE

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SummaryMore than a decade after the free-radical-theory of ovarian aging, researchers confirmed the importance of age-related oxidative threat to female fertility and moved to investigate the stress adaptive response in the ovarian follicle components. In this context a potential role for SIRT1, a NAD + -dependent deacetylase and key antiaging molecule, has arisen as guardian of the redox state and regulator of hormone secretion in the follicle. This review summarizes current knowledge on the role of this sirtuin in the ovarian follicle with particular emphasis to its relevance to the stress adaptive response during aging and potential implication in fertility preservation strategies.

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“…Higher adiposity leads to hormonal dysregulation, decreased primordial follicle numbers at the initiation of follicular development, lower ovulation rates, a reduced number of cleaved blastocysts developing to eight cell stage and reduced implantation rates, and ultimately impaired reproductive function (11,16,17,22,33,35,61). Similarly, in experimental models, obesity leads to decreased primordial and preovulatory follicle numbers, increased follicular atresia and changes in steroidogenesis via decreased steroidogenic acute regulatory protein, and increased Cyp11a1 protein content in ovarian tissue (7,16,23,37,38,53,61). Evidence of lipid accumulation, endoplasmic reticulum stress, and oxidative stress in ovaries from obese dams compared with lean controls may result partially in altered oocyte maturation, increased anovulation, and decreased in vivo fertilization rates (7,9,47,53,64,65).…”

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confidence: 99%

Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1

Ruebel

Shankar

Gaddy

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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A. Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1. Am J Physiol Endocrinol Metab 311: E269 -E277, 2016. First published June 7, 2016 doi:10.1152/ajpendo.00524.2015.-Obesity impairs reproductive functions through multiple mechanisms, possibly through disruption of ovarian function. We hypothesized that increased adiposity will lead to a proinflammatory gene signature and upregulation of Egr-1 protein in ovaries from obese (OB; n ϭ 7) compared with lean (LN; n ϭ 10) female Sprague-Dawley rats during the peri-implantation period at 4.5 days postcoitus (dpc). Obesity was induced by overfeeding (40% excess calories for 28 days) via total enteral nutrition prior to mating. OB dams had higher body weight (P Ͻ 0.001), greater fat mass (P Ͻ 0.001), and reduced lean mass (P Ͻ 0.05) and developed metabolic dysfunction with elevated serum lipids, insulin, leptin, and CCL2 (P Ͻ 0.05) compared with LN dams. Microarray analyses identified 284 differentially expressed genes between ovaries from LN vs. OB dams (Ϯ1.3 fold, P Ͻ 0.05). RT-qPCR confirmed a decrease in expression of glucose transporters GLUT4 and GLUT9 and elevation of proinflammatory genes, including CCL2, CXCL10, CXCL11, CCR2, CXCR1, and TNF␣ in ovaries from OB compared with LN (P Ͻ 0.05). Protein levels of PI3K and phosphorylated Akt were significantly decreased (P Ͻ 0.05), whereas nuclear levels of Egr-1 (P Ͻ 0.05) were increased in OB compared with LN ovaries. Moreover, Egr-1 was localized to granulosa cells, with the highest expression in cumulus cells of preovulatory follicles. mRNA expression of VCAN, AURKB, and PLAT (P Ͻ 0.05) correlated with %visceral fat weight (r ϭ 0.51, Ϫ0.77, and Ϫ0.57, respectively, P Յ 0.05), suggesting alterations in ovarian function with obesity. In summary, maternal obesity led to an upregulation of inflammatory genes and Egr-1 expression in peri-implantation ovarian tissue and a concurrent downregulation of GLUTs and Akt and PI3K protein levels.early growth response factor 1; gene expression; inflammation; obesity; reproduction IN THE US, 60% OF WOMEN OF REPRODUCTIVE AGE are either overweight or obese, which predisposes them to higher risk of infertility and pregnancy complications (12,21,57,59,60) and potentially leads to adverse effects on offspring development. Higher adiposity leads to hormonal dysregulation, decreased primordial follicle numbers at the initiation of follicular development, lower ovulation rates, a reduced number of cleaved blastocysts developing to eight cell stage and reduced implantation rates, and ultimately impaired reproductive function (11,16,17,22,33,35,61). Similarly, in experimental models, obesity leads to decreased primordial and preovulatory follicle numbers, increased follicular atresia and changes in steroidogenesis via decreased steroidogenic acute regulatory protein, and increased Cyp11a1 protein content in ovarian tissue (7,16,23,37,38,53,61). Evidence of lipid accumulation, endoplasmic reticulum stress, and oxidative stress in ova...

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Obesity accelerates ovarian follicle development and follicle loss in rats

Cited by 130 publications

References 56 publications

Maternal Overweight Disrupts the Sexual Maturation of the Offspring

Maternal Overweight Disrupts the Sexual Maturation of the Offspring

Follicle aging: a question of stress?

Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1

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