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Embryos were recovered from diabetic rats on day 5 of pregnancy and incubated in vitro for up to 72 h. Compared to control embryos, blastocysts from diabetic rats showed a marked impairment in growth that resulted at 48 h in a higher rate of degeneration and a lower morphological score in the developing population. After 72 h in vitro, fewer developing blastocysts from diabetic rats formed trophoblastic outgrowths and fewer of those implanted developed an inner cell mass when compared with the control group. When assessed for their cell content, blastocysts from diabetic rats contained fewer cells than control embryos at the start of the culture. This difference persisted, and even worsened, during the ensuing incubation period. The increasing cellular deficiency in blastocysts from diabetic rats was primarily located to their inner cell mass lineage but trophoblast growth was also affected. When trophoblast outgrowths were compared for their surface area and number of nuclei, those collected from diabetic rats were smaller, contained fewer nuclei and had a higher proportion of giant nuclei than control outgrowths. Our data thus demonstrate that despite their removal from the abnormal intra-uterine environment, blastocysts from diabetic rats remain functionally affected by their early exposure and fare less well than control embryos cultured under the same standard conditions.

In vitro study of the carry-over effect associated with early diabetic embryopathy in the rat