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

Fabian, Denis; Kubandová, Janka; Číkoš, Štefan; Burkuš, Ján; Fabianová, Kamila; Račeková, Enikő; Czikková, S.; Koppel, Juraj

doi:10.1016/j.theriogenology.2014.10.025

Cited by 12 publications

(20 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…According to the “hypothesis of developmental origins of adult diseases” ( 41 ), such genomic changes might have significant impacts on the further development of the conceptus or the health of the offspring. A decrease in body weight and fat in mouse offspring delivered from obese dams, shown in our previous study ( 14 ), might also be correlated with such changes.…”

Section: Discussionsupporting

confidence: 53%

“…The aim of the present study was to test the hypothesis that leptin could be one of the direct mediators of the previously documented negative effects of maternal obesity on early embryonic development and the incidence of apoptosis in blastocysts ( 13 , 14 ). Both apoptosis-inducing and apoptosis-inhibiting effects of leptin have been reported in various cell lineages: leptin increased the incidence of apoptosis in adipocytes or ovarian granulosa cells, although leptin also enhanced the survival of leukocytes, pancreatic, and endometrial cells [reviewed in Ref.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Responses of Mouse Preimplantation Embryos to Leptin In Vitro in a Transgenerational Model for Obesity

et al. 2017

Self Cite

View full text Add to dashboard Cite

The aim of the present study was to test the hypothesis that leptin can directly mediate the negative effect of maternal obesity on preimplantation embryos. As previously shown, maternal obesity retards early embryonic development in vivo and increases the incidence of apoptosis in blastocysts. When two-cell embryos isolated from control and obese mice were transferred to identical (leptin free) conditions in vitro, no differences in any growth or quality parameters were recorded, including apoptosis incidence in blastocysts. Embryos isolated from control mice responded to transfer to environments with a high concentration of leptin (10 ng/mL) with a significant increase in arrest at the first or subsequent cell cycle. However, the majority of non-arrested embryos developed into blastocysts, showing morphology comparable to those cultured in the leptin-free group. On the other hand, the exposure of embryos isolated from obese mice to high leptin concentration in vitro did not retard their development. Furthermore, these embryos developed into blastocysts, showing a lower incidence of apoptosis. In vivo-developed blastocysts recovered from obese mice showed elevated expression levels of the proapoptotic gene BAX and the insulin-responsive glucose transporter gene SLC2A4. In conclusion, elevated leptin levels have both positive and negative effects on preimplantation embryo development in vitro, a response that likely depends on the body condition of the embryo donor. Moreover, these results suggest that leptin acts as a survival factor rather than an apoptotic inductor in embryonic cells. Since no elevations in the expression of the leptin receptor gene (LEPR) or fat metabolism-associated genes (PLIN2, SLC27A4) were recorded in blastocysts recovered from obese mice, the role of leptin in mediating the effects of obesity on embryos at the peripheral level is likely lower than expected.

show abstract

Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

The Responses of Mouse Preimplantation Embryos to Leptin In Vitro in a Transgenerational Model for Obesity

et al. 2017

Self Cite

View full text Add to dashboard Cite

show abstract

“…In our previous studies we showed that the amount of maternal body fat or maternal restraint stress can significantly affect the quality of oocytes and in vivo developed preimplantation embryos (Burkuš et al 2013(Burkuš et al , 2015Kubandová et al 2014;Fabian et al 2015). In this study, we investigated the effect of stress on blastocyst quality in the context of maternal physiological status.…”

Section: Introductionmentioning

confidence: 97%

The effect of maternal stress on blastocyst quality depends on maternal physiological status

Janštová

Burkuš²,

Kubandová³

et al. 2017

gpb

Self Cite

View full text Add to dashboard Cite

The effect of maternal stress on blastocyst quality, with respect to maternal metabolic status, was investigated in this study. We exposed female mice with different amounts of body fat to restraint stress and examined their blastocyst quality. Blood concentrations of corticosterone, leptin, adiponectin, insulin and glucose were measured in these females. Significantly lower stress-induced corticosterone elevations were observed in females with high and low amounts of body fat, indicating that the stress response was altered in these females. The basal leptin concentrations were significantly higher in females with high amounts of body fat than in females with low amounts of body fat, and stress induced different responses in these two groups of females. Our results showed that maternal stress can significantly increase the proportion of blastocysts that contain dead (apoptotic) cells in females with high and medium amounts of body fat. In females with low amounts of body fat, the proportion of blastocysts containing dead (apoptotic) cells was already increased before the stress exposure, and application of stress did not significantly change this parameter. Our results showed that the effects of maternal stress on early embryos can depend on the actual physiological status of the maternal organism exposed to stress.

show abstract

“…Previous studies in this model (Kubandová et al 2014a;Kubandová et al 2014b;Fabian et al 2015;Janštová et al 2017;Chi et al 2000;Jungheim et al 2010 Therefore, it might be hypothesized that metabolic status does not affect mouse reproduction through changes in basal ovarian steroid or IGF-I release, although metabolism-dependent changes in the upstream regulators of these hormones, the ovarian response to these upstream regulators, or to P4, T, or IGF-I ought not to be excluded. The latter hypothesis is confirmed by the fact that obesity in mice is associated with both impaired fertility and alterations in IGF-I receptors in the reproductive system (Chi et al 2000;Jungheim et al 2010).…”

Section: Does Metabolic State Control Mice Fecundity Via Ovarian P4 mentioning

confidence: 89%

“…For these studies, we used the previously validated two-generation model (Kubandová et al 2014a;Kubandová et al 2014b;Fabian et al 2015;Janštová et al 2017) that resulted in the production of offspring , which manifested the signs of obesity at the time of sexual adulthood. All experiments were performed on mice dams of the outbred ICR strain (Velaz, Prague, Czech Republic).…”

Section: Animals and Experimental Designmentioning

confidence: 99%

Metabolic state can define the ovarian response to environmental contaminants and medicinal plants

Sirotkin

Fabian

Babeľová

et al. 2017

Appl. Physiol. Nutr. Metab.

Self Cite

View full text Add to dashboard Cite

Environmental contaminants and medicinal plants can affect reproductive processes. The aim of this study was to investigate the effect of maternal metabolic status on the response of mouse ovaries to the environmental contaminants benzene and xylene, as well as to extracts of the medicinal plant yucca. Ovaries isolated from normal-lean and slightly obese mice were cultured with or without 0.1% benzene or xylene for 24 h. Similarly, ovaries isolated from normal-lean, slightly obese, and significantly obese mice were cultured for 24 h with or without an extract of Yucca shidigera (YS, 10 μ g/mL). We found that the metabolic status did not influence the release of basal progesterone (P4), testosterone (T), or insulin-like growth factor I (IGF-I), but obesity influenced the effects of the environmental contaminants and YS. Benzene reduced P4 output in ovaries from obese but not normal-lean mice; it also reduced IGF-I (but not T) release from ovaries irrespective of the metabolic status. Xylene dramatically increased P4 and T (but not IGF-I) release by ovaries from normal-lean mice, but there were no changes in P4 and only small increases in T output in obese mice. YS increased P4 (but not T or IGF-I) release in normal-lean and slightly obese animal ovaries, whilst significant obesity was associated with a lack of P4 response to YS. Obesity might affect the basal ovarian release of T or IGF-I and increases the sensitivity of ovaries to the action of benzene but decreases their responsiveness to xylene and YS.

show abstract

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

Cited by 12 publications

References 53 publications

The Responses of Mouse Preimplantation Embryos to Leptin In Vitro in a Transgenerational Model for Obesity

The Responses of Mouse Preimplantation Embryos to Leptin In Vitro in a Transgenerational Model for Obesity

The effect of maternal stress on blastocyst quality depends on maternal physiological status

Metabolic state can define the ovarian response to environmental contaminants and medicinal plants

Contact Info

Product

Resources

About