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

Abstract

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.

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

“…A two-generation model based on the overnutrition of experimental animals during intrauterine and early postnatal development, previously developed in our laboratory ( 13 ), was employed to produce mice with an obesity-like phenotype. Obese mice, derived from dams fed a high-energy diet, regularly show significantly elevated body weight and body fat, with massive fat deposits in the abdominal and perirenal areas and display increased plasma glucose, insulin, and leptin levels ( 13 , 19 ).…”

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

“…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).…”

“…2012; Broughton andMoley 2017, Štochmaľová et al 2015;Vlčková et al 2017;Kubandová et al 2014a;Kubandová et al 2014b;Janštová et al 2017). Therefore, a functional interrelationship between YS and obesity in the control of these processes might be expected.…”

“…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).…”

“…Fat per se is probably not the main cause of these differences because in our experiments the fat was carefully removed from the ovaries before culture. More probable is the influence of body fat on ovaries before their isolation, either via a non-specific effect on metabolism and resistance of cells to environmental toxins, or through the action of fat-derived adipokines whose influence on ovarian functions in mammals including mice is well documented (Kubandová et al 2014a;Kubandová et al 2014b;Janštová et al 2017, Sirotkin. 2011Allen et al 2016;Cheng et al 2016).…”