Congenital malformations induced by alloxan diabetes in mice and rats

Takano, Kiichi; Nishimura, Hideo

doi:10.1002/ar.1091580310

Cited by 23 publications

(10 citation statements)

References 20 publications

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“…Congenital anomalies in the offspring of diabetic mothers have been investigated from various standpoints, such as the treatment of diabetes mellitus [1][2][3][4][5][6][7][8], environmental fac tors [9][10][11][12][13] and genetic factors [14][15][16][17][18],…”

Section: Introductionmentioning

confidence: 99%

Relationship between Associations of NOR and Chromosomal Anomalies in the Abnormal Embryos of Nonobese Diabetic and STZ-Diabetic Mouse

Tatewaki

Hashimoto²,

Tanigawa³

et al. 1995

Neonatology

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Associations of nucleolar organizing regions (NORs) in the postimplantation stage embryos of nonobese diabetic (NOD) mice, and diabetic ICR mice induced by streptozotocin (ST), were studied to investigate the possible cause of the numerical anomalies of the chromosomes in their abnormal embryos. The incidence of NOR associations in abnormal embryos from diabetic NOD (NOD-DM) and STZ-diabetic mice was 11.7 and 7.7%, respectively. This incidence was significantly higher than that (1.2%, p < 0.05) of normal embryos from ICR mice which were used as control. From the results analyzed cytogenetically it was suggested that the higher incidence of chromosomal numerical anomalies in the embryos from NOD-DM and STZ-diabetic mice were caused by the chromosomal nondisjunction induced by associations of NORs. Furthermore, it was suggested that NOD-DM embryos have a tendency to increase the associations of NOR in a diabetic condition together with other factors such as autoimmune disease, however a diabetic condition alone induced chromosomal anomalies. Regarding relationships between the incidence of associations of NOR and the types of malformed embryos, it was also clear that all of the abnormal embryos from NOD-DM and STZ-diabetic mice had a high incidence of associations of NOR, and that the incidence was not related to the types of congenital anomalies. Furthermore, in the mal-developed tissue of embryos from STZ-diabetic mice, many chromosomal anomalies were found (26.6%), and the incidence was similar to that of whole embryos (22.6%). Unexpectedly, the incidence of associations of NOR in the maldeveloped tissue was not higher than that of whole embryos. As the results in this study suggest, the numerical anomalies induced by association of NOR seemed to be a causal factor of the disorder of morphogenesis, rather than a resulting phenomenon in abnormal embryos from diabetic mothers.

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Section: Introductionmentioning

confidence: 99%

Relationship between Associations of NOR and Chromosomal Anomalies in the Abnormal Embryos of Nonobese Diabetic and STZ-Diabetic Mouse

Tatewaki

Hashimoto²,

Tanigawa³

et al. 1995

Neonatology

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“…Many attempts have been made to attrib ute abnormalities to environmental factors such as hyperglycemia and hyperketonemia [9][10][11][12][13] and to genetic factors [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Chromosome Analysis of Postimplantation Stage Embryos for Studying Possible Causes of Developmental Abnormalities in Nonobese Diabetic Mice

Tatewaki¹,

Otani²,

Ando

et al. 1991

Neonatology

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The chromosomes of postimplantation stage embryos of nonobese diabetic (NOD) mice were analyzed to investigate the causal mechanism of congenital anomalies in diabetic pregnancies. Postimplantation stage embryos (day 12 of gestation) in diabetic (NOD-DM) and nondiabetic (NOD-N) NOD mice had either a high or low incidence of chromosomal abnormalities. A large majority of externally normal embryos from NOD-DM and NOD-N mice had low incidences. A high incidence of chromosomal abnormalities was found in externally abnormal embryos of NOD-DM and NOD-N mice, and in a smaller number of externally normal NOD-N and NOD-DM embryos. No control ICR embryo manifested a high incidence of chromosomal abnormalities. In the NOD-DM embryos, the chromosomes appeared to be influenced by long-term maternal diabetic conditions, while high incidences of chromosomal abnormalities in the NOD-N embryos suggested a probable cause by other factor(s) (e.g. a genetic predisposition) or by a very mild diabetic condition because the NOD-N mice were prediabetic.

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“…As yet, this hypothesis has not been examined in vivo. Indeed, relatively few attempts have been made to correlate precisely timed exposures of offspring to an abnormal metabolic environment in utero with subsequent developmental abnormalities (4)(5)(6)(7)(8)(9)(10)(11). In most of these, the period of metabolic disruption has been too long relative to the rapid development of the conceptus and/or too imprecisely documented to allow exact temporal assessments.…”

Section: Introductionmentioning

confidence: 99%

Fuel-mediated teratogenesis. Use of D-mannose to modify organogenesis in the rat embryo in vivo.

Buchanan¹,

Freinkel²,

Lewis³

et al. 1985

J. Clin. Invest.

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Congenital malformations induced by alloxan diabetes in mice and rats

Cited by 23 publications

References 20 publications

Relationship between Associations of NOR and Chromosomal Anomalies in the Abnormal Embryos of Nonobese Diabetic and STZ-Diabetic Mouse

Relationship between Associations of NOR and Chromosomal Anomalies in the Abnormal Embryos of Nonobese Diabetic and STZ-Diabetic Mouse

Chromosome Analysis of Postimplantation Stage Embryos for Studying Possible Causes of Developmental Abnormalities in Nonobese Diabetic Mice

Fuel-mediated teratogenesis. Use of D-mannose to modify organogenesis in the rat embryo in vivo.

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