J. Vesela et al., EFFECTS OF HEALTHY PSEUDOPREGNANT MILIEU ON DEVELOPMENT OF 2-CELL SUBDIABETIC MOUSE EMBRYOS, Journal of Reproduction and Fertility, 100(2), 1994, pp. 561-565
Female mice were injected with a single dose of streptozotocin (65 mg
kg(-1)) 14-17 days before fertilization to investigate the significanc
e of impaired insulin secretion induced by subdiabetic streptozotocin
treatment on preimplantation embryo development. Subdiabetic mice (str
eptozotocin-treated) had significantly different glucose tolerance fro
m that of control animals, despite similar basal glycaemia. Morphologi
cal analysis of preimplantation embryos collected on day 2 of pregnanc
y revealed no significant changes in the number of two-cell embryos re
covered from streptozotocin-treated females compared with controls. Tw
o-cell embryos were transferred into the oviducts of healthy, synchron
ous pseudopregnant females and recovered 24-28 h later. Morphological
evaluation revealed a significantly greater percentage of degenerated
embryos from streptozotocin-treated females than from control females.
Morphological analysis of preimplantation embryos collected on day 2.
5 of pregnancy revealed no significant changes in the number of two- t
o four-cell embryos recovered from streptozotocin-treated females comp
ared with controls, but there was a significant increase in the number
of degenerated embryos in streptozotocin-treated females that did not
receive insulin therapy. Insulin (1-1.5 iu per 100 g) administered tw
ice a day to streptozotocin-treated mice significantly improved the al
tered development of embryos in both experiments. It is possible that
the impaired insulin secretion in female mice adversely affected the g
rowth of preimplantation embryos. Almost half of the morphologically n
ormal two-cell embryos isolated from subdiabetic females were incapabl
e of development to the eight-cell stage even in a non-diabetic matern
al environment. The morphologically distinct degenerative changes were
first detected at the time of the second mitotic cleavage.