Effects of streptozotocin‐induced diabetes on fetal development of the rat

Giavini, Erminio; Broccia, Maria Luisa; Roversi, G. D.; Vismara, Claudio

doi:10.1002/tera.1420340111

Cited by 41 publications

(33 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, also under these drastic conditions, the effects on the embryos are indicative of developmental delay more than of a clear teratogenic effect. Similar findings have been shown by our previous experience with in vivo and in vitro experiments on diabetes [8,32,34,[46][47][48]. In this respect, a very interesting and deep critical review of the literature (144 references) has recently been published by Kalter [49], in which the author says: 'So far as the experiments are concerned, it is abundantly clear that the induction of diabetes by chemicals is often inefficient, and that, when induced, diabetes is frequently not teratogenic.…”

Section: Discussionsupporting

confidence: 78%

“…Upon changing the strain of rats used in their experiments, this syndrome disappeared, showing a clear genetic predisposition in diabetes-induced malformations [6,7]. Apart from Eriksson's studies, the majority of experiments carried out on rats made diabetic with streptozotocin have not produced a significant increase in congenital malformations, and the major effect observed has been a developmental delay [8][9][10][11][12]. During the last decade, a number of studies have been carried out in vitro, using postimplantation mouse and rat embryos and rat serum as culture medium.…”

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Development of Rat Embryos Cultured in Serum from Diabetic Rats

Menegola¹,

Broccia²,

Giavini³

1998

Neonatology

View full text Add to dashboard Cite

Experimental studies carried out in vitro suggest a role of oxidative stress in diabetes-induced embryopathies. Glutathione is the main defense against free radicals in embryonic as it is in adult tissues. In this experiment, using postimplantation whole-embryo culture, we analyze: (1) the effects of serum from streptozotocin-induced diabetic rats on embryonic development and on glutathione distribution between the yolk sac and embryonic tissues and (2) the role of glutathione in preventing embryopathies (using the inhibitor of glutathione synthesis buthionine sulfoximine). Our data show that in rat embryos cultured in diabetic serum, the only observed effects are at the yolk sac level. No effects on the glutathione content were observed. The addition of buthionine sulfoximine reduced the glutathione content and produced signs of developmental delay in embryos cultured in diabetic serum, suggesting a role of the oxidative stress in producing diabetes-related embryotoxicity.

show abstract

Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 98%

Development of Rat Embryos Cultured in Serum from Diabetic Rats

Menegola¹,

Broccia²,

Giavini³

1998

Neonatology

View full text Add to dashboard Cite

show abstract

“…The hyperglycemic state has been shown to be associated with increased risk for embryonic dysmorphogenesis [28]. Increased incidence of malformations in the offspring of diabetic mothers with elevated HbA1c levels during early human pregnancy [29] and similar observations in rodent diabetic pregnancies [30][31][32] support these findings. Furthermore, since the time required for the induction of malformations is very short (24 h) in chick embryos as compared to mammalian embryos, e.g.…”

Section: Discussionmentioning

confidence: 67%

Shell-Less Chick Embryo Culture as an Alternative in vitro Model to Investigate Glucose-Induced Malformations in Mammalian Embryos

Datar¹,

Bhonde²

2005

Rev Diabetic Stud

View full text Add to dashboard Cite

■ AbstractWe have developed a simple shell-less chick embryo culture system to study glucose-induced malformations. This system involves the culturing of chick embryos from the second day to the fifth day of incubation, with associated yolk and thick and thin albumen outside the egg shell. The system allows the observation of embryonic development of chicks in a glass bowl. Developing embryos at 24 h, 48 h and 72 h incubation, corresponding to the Hamberger Hamilton (HH) stages from 7 to 21, were treated with two concentrations of glucose (50 mM and 100 mM) for 24 h. Glucose treatment resulted in a mortality rate of over 70% in younger embryos. Furthermore, a variety of malformations such as retarded growth, abnormal heart development, macrosomia, exencephaly, etc. were observed in older embryos, which were similar to those reported in mammalian embryos as a consequence of diabetic pregnancy. The glucose-induced malformations were found to be concentration-and stage-dependent, thus emphasizing the roles of the degree of hyperglycemia and the stage of embryonic development in diabetic growth anomalies. Here we demonstrate for the first time that the present system can be used (i) for experiments at early stages of chick embryo development and (ii) for assessing the effects of acute glucose toxicity similar to those reported for mammalian embryos in a hyperglycemic environment.

show abstract

“…The underlying metabolic disorder may predispose offspring to develop metabolic diseases in later life (Silveira et al 2007). Several animal studies demonstrated a developmental delay for embryos recovered from diabetic mothers (Giavini et al 1986, Moley et al 1991. Our study provides new insights into the effects of a maternal DM during the preimplantation period by analyzing the AGE formation in both, the mother and the developing embryo.…”

Section: Discussionmentioning

confidence: 82%

Accumulation of advanced glycation end products in the rabbit blastocyst under maternal diabetes

Haucke¹,

Simm²,

Henning³

et al. 2014

Reproduction

View full text Add to dashboard Cite

Diabetes mellitus (DM) during pregnancy is one of the leading causes of perinatal morbidity and birth defects. The mechanism by which maternal hyperglycemia, the major teratogenic factor, induces embryonic malformations remains unclear. Advanced glycation end products (AGEs) are known to accumulate during the course of DM and contribute to the development of diabetic complications. Employing a diabetic rabbit model, we investigated the influence of maternal hyperglycemia during the preimplantation period on AGE formation (pentosidine, argpyrimidine, and N 3 -carboxymethyllysine (CML)) in the reproductive tract and the embryo itself. As a consequence of type 1 DM, the AGE levels in blood plasma increased up to 50%, correlating closely with an AGE accumulation in the endometrium of diabetic females. Embryos from diabetic mothers had increased protein-bound CML levels and showed enhanced fluorescent signals for AGE-specific fluorescence in the blastocyst cavity fluid (BCF). The quantification of CML by HPLC-mass spectrometry (MS/MS) showed a higher amount of soluble CML in the BCF of blastocysts from diabetic rabbits (0.26G0.05 mmol/l) compared with controls (0.18G0.02 mmol/l). The high amount of AGEs in blastocysts from diabetic mothers correlates positively with an increased AGER (receptor for AGE (RAGE)) mRNA expression. Our study gives alarming insights into the consequences of poorly controlled maternal diabetes for AGE formation in the embryo. Maternal hyperglycemia during the preimplantation period is correlated with an increase in AGE formation in the uterine environment and the embryo itself. This may influence the development of the embryo through increased AGE-mediated cellular stress by RAGEs.

show abstract

Effects of streptozotocin‐induced diabetes on fetal development of the rat

Cited by 41 publications

References 29 publications

Development of Rat Embryos Cultured in Serum from Diabetic Rats

Development of Rat Embryos Cultured in Serum from Diabetic Rats

Shell-Less Chick Embryo Culture as an Alternative in vitro Model to Investigate Glucose-Induced Malformations in Mammalian Embryos

Accumulation of advanced glycation end products in the rabbit blastocyst under maternal diabetes

Contact Info

Product

Resources

About