Decreased Inner Cell Mass Proportion in Blastocysts From Diabetic Rats

Pampfer, S.; Hertogh, R. De; Vanderheyden, I.; Michiels, B.; Vercheval, M

doi:10.2337/diab.39.4.471

Cited by 115 publications

(103 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another finding was that a diabetic environment hampers embryonic growth, measured as crown-to-rump length. This observation is in line with earlier studies showing decreased inner cell mass in blastocysts from diabetic rats (44). The crown-to-rump length is likely a reflection of a general environmental stress factor during embryonic growth, whereas the fetal malformation difference between H and U strains relates to specific genetic susceptibilities expressed under diabetic conditions.…”

Section: Discussionsupporting

confidence: 80%

Increased mRNA levels of Mn-SOD and catalase in embryos of diabetic rats from a malformation-resistant strain.

et al. 2000

View full text Add to dashboard Cite

Previous studies have suggested that reactive oxygen species (ROS) are mediators in the teratogenic process of diabetic pregnancy. In an animal model for diabetic p r e g n a n c y, offspring of the H rat strain show minor dysmorphogenesis when the mother is diabetic, whereas the offspring of diabetic rats of a sister strain, U, display major morphologic malformations. Earlier studies have shown that embryonic catalase activity is higher in the H than in the U strain, and maternal diabetes increases this difference in activity. The aim of this study was to characterize the influence of genetic predisposition on diabetic embryopathy by comparing the mRNA levels of ROS-metabolizing enzymes in the two strains. We determined the mRNA levels of catalase, glutathione peroxidase, -g l u t a m y l c y s t e i n -s y n t h e t a s e , glutathione reductase, and superoxide dismutase (CuZn-SOD and Mn-SOD) in day 11 embryos of normal and diabetic H and U rats using semiquantitative reverse transcription-polymerase chain reaction. The mRNA levels of catalase and Mn-SOD were increased in H embryos as a response to maternal diabetes, and no d i fferences were found for the other genes. Sequence analysis of the catalase promoter indicated that the d i fference in mRNA levels may result from diff e r e n t regulation of transcription. Sequence analysis of the catalase cDNA revealed no differences between the two strains in the translated region, suggesting that the previously observed difference in the electrophoretic mobility in zymograms is due to posttranslational modifications. An impaired expression of scavenging enzymes in response to ROS excess can thus be an integral part of a genetic predisposition to embryonic dysmorphogenesis. D i a b e t e s 4 9 :1 0 1-107, 2000 M aternal type 1 diabetes during pregnancy has been known for many years to be associated with an increased risk for congenital malformations in the offspring (1-4). Clinical studies have estimated the risk for a malformed fetus in a t y p e 1 diabetic pregnancy to be in the range of 5-10% (5-9). The malformations are induced before the 7th postconceptional week in human diabetic pregnancy (10). In rats, the teratogenic process is believed to occur during organogenesis (11). Recent reports, however, indicate that a diabetic environment may decrease the inner cell mass (12) and that a high glucose concentration can lead to increased apoptosis already in the preimplantation embryo (13). The teratogenic process and its predisposing factors are not known in detail. In pregnancies with poorly controlled diabetes, however, there is a correlation between the level of H b A 1 c in maternal blood and the risk for having a malformed child (5,14,15).The hypothesis has been put forward that an excess of reactive oxygen species (ROS) mediates the teratogenicity of diabetic pregnancy (16)(17)(18)(19). The oxygen radicals may be harmful to the cell and its functions by reacting with unsaturated fatty acids in membranes, yielding lipid peroxides and causing decreased membran...

show abstract

Section: Discussionsupporting

confidence: 80%

Increased mRNA levels of Mn-SOD and catalase in embryos of diabetic rats from a malformation-resistant strain.

et al. 2000

View full text Add to dashboard Cite

show abstract

“…IGF-I mRNA could not be detected in preimplantation embryos in the present study, which is consistent with the absence of this mRNA in preimplantation mouse embryos (Rappolee et al, 1990 (Bavister, 1988 (Pampfer et al, 1990;Beebe and Kaye, 1991).…”

Section: Discussionsupporting

confidence: 80%

Possible roles of insulin and insulin-like growth factors in rat preimplantation development: investigation of gene expression by reverse transcription-polymerase chain reaction

Zhang¹,

Kidder²,

Watson³

et al. 1994

Reproduction

View full text Add to dashboard Cite

“…Using nuclear fragmentation within intact cell membranes as a marker, a fourfold increase has been detected in the incidence of cell death in the ICM lineage of blastocysts recovered from diabetic rats. 17,18 Blastocysts from diabetic rats 19 and mice 20 also contain a higher proportion of cells with nuclear chromatin degradation, as revealed by TUNEL staining. Excess cell death in these blastocysts was corrected by achieving maternal normoglycemia through insulin administration.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis at the time of embryo implantation in mouse and rat

1999

Self Cite

View full text Add to dashboard Cite

The aim of this review is to summarize the information currently available regarding the occurrence of apoptosis in the developing embryo and in the receptive uterus during the peri-implantation period of gestation. Cell death is detected in the inner cell mass of late pre-implantation embryos as the result of an eliminative process that helps trim the embryonic cell lineages of surplus or dysfunctional stem cells. Cell death is also detected in the epiblastic core of early postimplantation embryos, where the process is implicated in the formation of the pro-amniotic cavity. On the maternal side, uterine epithelial cells situated around the attachment site undergo cell death during the initial phase of implantation in order to facilitate embryo anchorage and access to maternal blood supply. Uterine stromal cells closest to the implantation chamber first transform into decidual cells and then commit suicide to make room for the rapidly growing embryo. Although apoptosis is well recognized as a crucial determinant of successful peri-implantation development, our understanding of the cellular and molecular mechanisms regulating this process clearly lags behind the comprehension of cell death control in other systems.

show abstract

Decreased Inner Cell Mass Proportion in Blastocysts From Diabetic Rats

Cited by 115 publications

References 31 publications

Increased mRNA levels of Mn-SOD and catalase in embryos of diabetic rats from a malformation-resistant strain.

Increased mRNA levels of Mn-SOD and catalase in embryos of diabetic rats from a malformation-resistant strain.

Possible roles of insulin and insulin-like growth factors in rat preimplantation development: investigation of gene expression by reverse transcription-polymerase chain reaction

Apoptosis at the time of embryo implantation in mouse and rat

Contact Info

Product

Resources

About