Effects of streptozotocin- and alloxan-induced diabetes mellitus on mouse follicular and early embryo development

Abstract

Mice were made diabetic by intraperitoneal injection of streptozotocin or alloxan. Germinal vesicle breakdown in the ovarian follicles at 8 h after hCG in control animals (57%) was significantly greater than in streptozotocin-(24%) and alloxan\x=req-\ (42%) diabetic animals (P < 0\m=.\001). This delay in oocyte maturation was reversible by in-vivo insulin administration to diabetic mice. A developmental delay was also found for embryos recovered from diabetic mice. This developmental delay extended into the 72 h in-vitro cultures. Compared to control embryos, those from alloxan-and streptozotocin-treated mice demonstrated marked impairment in development as assessed by (1) distribution of developmental cell stages at each observation period and (2) rates of development which increasingly diverged at each observation period.In diabetic mice treated with insulin in vivo, the percentage of 2-cell embryos recovered increased. Furthermore, in streptozotocin-and alloxan-animals treated with insulin, the rate of in-vitro development of embryos, as well as their developmental stage distribution improved. We therefore suggest that uncontrolled diabetes mellitus, as well as contributing to the development of congenital malformations, may deleteriously affect reproductive performance both before fertilization and at the very earliest gestational stages.

The impact of obesity on egg quality

“…Many studies using mouse models of type I diabetes have shown the negative impact of hyperglycemia alone on oocyte maturation. Oocytes from type I diabetic mice exhibit delays in maturation [36][37][38] accompanied by spindle defects and chromosome misalignment during oocyte maturation [37]. Maternal type I diabetes also causes increased granulosa cell apoptosis [37].…”

Protective Effects of Aloe Vera on Superovulated Oocytes and Folliculogenesis in Diabetic Mice

“…It is reported that overnight culture of denuded oocytes lead to complete meiosis (98%) at control level, while in COC culture, MII reached oocytes were significantly lowered compared to controls [11]. Powers et al [12], suggest that the decreasing in ovulation rate may be due to impairment of nitric oxide protection, due to a defect in the blood follicle barrier in diabetic ovaries.…”

Infertile marriage in patients with diabetes mellitus

“…Исследования на лабораторных животных показали, что даже кратковременное воздействие гипергликемии у бере-менных самок приводит к задержке развития эмбрионов [36,37]. Эмбрионы, полученные от животных в состоянии острой гипергликемии, вызванной стрептозотоцином или аллоксаном, отличались от эмбрионов здоровых особей сниженной скоро-стью дробления [36].…”

“…Эмбрионы, полученные от животных в состоянии острой гипергликемии, вызванной стрептозотоцином или аллоксаном, отличались от эмбрионов здоровых особей сниженной скоро-стью дробления [36]. Было показано, что гипергликемия также оказывает отрицательное влияние на питание и энергетические ресурсы эмбриона в преимплантационный период: у эмбрионов от самок с СД отмечалось снижение утилизации глюкозы, ко-торое было непосредственно связано со снижением транспорта глюкозы как на уровне мРНК, так и на уровне транспортных белков Glut [38].…”