Paternal diet-induced obesity impairs embryo development and implantation in the mouse

Mitchell, Megan; Bakos, Hassan W.; Lane, Michelle

doi:10.1016/j.fertnstert.2010.09.038

Cited by 146 publications

(129 citation statements)

References 54 publications

(60 reference statements)

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“…Interestingly if embryos were maintained in culture for a further 24 h until day 5, this delay in development dissipated (Table 3). A delay to embryonic development that is attenuated by the blastocyst stage is reminiscent of the embryo phenotype observed for embryos derived directly from HFD fed founders themselves [9,11,12,32].…”

Section: Female Offspring Produce Embryos With Delayed Developmentmentioning

confidence: 86%

“…This alteration to early cellular partitioning potentially indicates reduced embryo quality. Previous studies demonstrate that an alteration to the number of both TE and ICM cells in the blastocyst are associated with reduced implantation rates [9,[39][40][41], although implantation is presumably more sensitive to TE cell number. Overall, embryos from female offspring sired by obese fathers displayed delayed development and impaired quality despite the offspring themselves being fed a control diet, mimicking the developmental profile of embryos sired directly by HFD males themselves [9,12,32,42].…”

Section: Discussionmentioning

confidence: 99%

“…More than one-third of men of reproductive age in the United States are classified as obese [1]. Paternal obesity not only impairs male fertility by impacting sperm count, motility and chromatin integrity [2][3][4][5][6][7] but also reduces subsequent embryo development, implantation rates, pregnancy success and live birth rates [8][9][10][11][12]. Interestingly metabolic syndrome, which includes obesity, in fathers is associated with polycystic ovary syndrome in daughters [13].…”

Section: Introductionmentioning

confidence: 99%

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Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Fullston

Shehadeh

Sandeman

et al. 2015

J Assist Reprod Genet

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Purpose To investigate the impacts that a paternal high fat diet (HFD) has on embryology, ovarian/cumulus cell gene expression and COC metabolism from female offspring, using a mouse model. Methods Founder male mice were either fed a control diet (CD) or a HFD for 12 weeks. The HFD induced obesity but not diabetes, and founder males were then mated to normal weight CD fed female mice. Female offspring were maintained on a CD, super-ovulated, mated and the resultant zygotes were cultured to the blastocyst stage for embryo morphology, blastocyst cell number and apoptosis assessment. Ovaries and cumulus cells from offspring were collected for gene expression analysis of selected genes that maintain chromatin remodeling and endoplasmic reticulum (ER), metabolic and inflammatory homeostasis. Cumulus/oocyte complexes were also investigated for glucose uptake and lipid accumulation. Results Female offspring sired by obese fathers produced embryos with delayed development and impaired quality, displayed increases in ovarian expression of Glut1, Glut3 and Glut4, and an increase in cumulus cell expression of Glut4. Interestingly their COCs did take up more glucose, but did accumulate more lipid. Conclusions A paternal HFD is associated with subfertility in female offspring despite the offspring being fed a CD and this subfertility is concomitant with ovarian/cumulus cell molecular alterations and increased lipid accumulation.

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Section: Female Offspring Produce Embryos With Delayed Developmentmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Fullston

Shehadeh

Sandeman

et al. 2015

J Assist Reprod Genet

Self Cite

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“…[27][28][29][30] Recent evidence from both animal and human studies indicates that male obesity and high-fat diets result in impaired reproductivity, affecting the molecular and physical structure of sperm as well as the health of the developing fetus and subsequent offspring. 27,[31][32][33][34][35][36][37][38][39] In a recent animal study, Rato et al 39 reported that the testicular physiology is sensitive to alterations of whole-body metabolism and that the testicular metabolism can be disturbed by high-energy diets. Disruption of testicular metabolism is associated with decreased sperm quality.…”

Section: Introductionmentioning

confidence: 99%

Nutritional modifications in male infertility: a systematic review covering 2 decades

et al. 2015

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Context: Studies suggest that appropriate nutritional modifications can improve the natural conception rate of infertile couples. Objectives: The purpose of this study was to review the human trials that investigated the relation between nutrition and male infertility. Data Sources: A comprehensive systematic review of published human studies was carried out by searching scientific databases. Article selection was carried out in accordance with Preferred Reporting Items for Systematic Reviews and MetaAnalyses. The American Dietetic Association Research Design and Implementation Checklist was also used for quality assessment. Data Extraction: A total of 502 articles were identified, of which 23 studies met the inclusion criteria. Data Synthesis: Results indicated that a healthy diet improves at least one measure of semen quality, while diets high in lipophilic foods, soy isoflavones, and sweets lower semen quality. Conclusion: The role of daily nutrient exposure and dietary quality needs to be highlighted in male infertility. Mechanistic studies addressing the responsible underlying mechanisms of action of dietary modifications are highly warranted.

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“…Indeed, some studies of third party reproduction indicate that obesity has a negative impact on development through its effects on the uterine environment [12][13][14][15], and recent studies suggest obesity may be affecting sperm function as well [16][17][18][19]. This review will focus solely on how obesity and insulin resistance affect the oocyte.…”

mentioning

confidence: 99%

The impact of obesity on egg quality

Purcell

Moley

2011

J Assist Reprod Genet

136

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Obesity in women is a concern in many countries. This causes numerous health issues; however, this review focuses on the impact of obesity on women's reproduction, and in particular the oocyte. Data from infertility clinics and experimental animal models that address the effects of obesity are presented. Bidirectional communication and metabolic support from the surrounding cumulus cells are critical for oocyte development, and the impact of obesity on these cells is also addressed. Both oocyte maturation and metabolism are impaired due to obesity, negatively impacting further development. In addition to reproductive hormones, obesity induced elevations in insulin, glucose, or free fatty acids, and changes in adipokines appear to impact the developmental competence of the oocyte. The data indicate that any one of these hormones or metabolites can impair oocyte developmental competence in vivo, and the combination of all of these factors and their interactions are the subject of ongoing investigations.

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Paternal diet-induced obesity impairs embryo development and implantation in the mouse

Cited by 146 publications

References 54 publications

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Nutritional modifications in male infertility: a systematic review covering 2 decades

The impact of obesity on egg quality

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