-transparent.png){kind=logo}
To investigate the significance of impaired insulin secretion on preimplantation embryo development, outbred ICR female mice received a single injection of streptozotocin 130 mg (low) and 160 mg (subdiabetic) kg(-1), 14-17 days before fertilization. Preimplantation embryos were collected on day 3 of pregnancy, four to eight-cell embryos were cultured in vitro 48 h (day 5) and their cell number was estimated. After spontaneous ovulation, the significantly different distribution pattern in comparison with the controls was detected only in preimplantation embryos isolated from subdiabetic (160 mg x kg(-1) streptozotocin) mice. Furthermore, the incidence of degenerated embryos was significantly increased after 48 h in vitro cultivation. The analysis of cell number distribution in embryos after cultivation in vitro indicated a significant delay in cell proliferation in both experimental groups (130 and 160 mg x kg(-1) streptozotocin) in comparison with control mice. After superovulation, the only significant difference was found in the distribution pattern of embryos isolated on day 3 of pregnancy from subdiabetic (160 mg x kg(-1) streptozotocin) mice. No significant differences were found after embryo cultivation in vitro. It could be concluded that, in outbred ICR mice, lower streptozotocin treatment (130 mg x kg(-1)) influenced only cell distribution of in vitro cultured embryos after spontaneous ovulation. In ICR mice, marked changes in preimplantation embryo development were detected only after subdiabetic (160 mg x kg(-1)) streptozotocin treatment. During in vitro cultivation delayed effects of impaired insulin secretion resulted in an increase of embryo degeneration at the time after the third mitotic cleavage. Our results indicate that the effects of impaired maternal insulin secretion on preimplantation embryo development in mice are marked and consistent after spontaneous ovulation. Superovulation apparently disguises subtle changes in preimplantation embryo development after low and subdiabetic streptozotocin treatment.
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
January 1996,
Physiological research,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
December 2011,
Reproductive toxicology (Elmsford, N.Y.),
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
October 2016,
Reproduction (Cambridge, England),
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
February 2009,
Lab animal,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
November 1983,
The Journal of experimental zoology,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
June 2012,
Fertility and sterility,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
January 1990,
Reproduction, fertility, and development,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
January 2016,
Seminars in reproductive medicine,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
December 2013,
Progress in biophysics and molecular biology,
J Mihalik, and
P Rehák, and
J Veselá, and
S Cikos, and
V Baran, and
J Koppel
June 2009,
Reproductive biology and endocrinology : RB&E,
