Diabetic environment and genetic predisposition as causes of congenital malformations in NOD mouse embryos

Otani, H.; Tanaka, O.; Tatewaki, Reiko; Naora, H.; Yoneyama, T.

doi:10.2337/diabetes.40.10.1245

Cited by 24 publications

(22 citation statements)

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“…Both genetic and environmental factors have been implicated in the pathogenesis of type 1 diabetes (Atkinson & Maclaren 1994;Tisch & McDevitt 1996), and maternal factors represent some of the most salient environmental influences during the earlier stages of life (for review, see Shanks & Lightman 2001). In our previous study, by transplanting NOD embryos into the ICR uterus, we investigated the interaction between genetic predisposition and the maternal diabetic environment in NOD embryos as causes of congenital malformation in the offspring from diabetic mothers (Otani et al 1991). Using the same experimental strategy, we also found that NOD maternal environment affects the onset and severity of insu-litis as well as incidence of overt diabetes in the offspring (Kagohashi et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…When a vaginal plug was confirmed in the following morning, this day was defined as day 0 of gestation (E0). Embryo transfer was performed utilizing well-established techniques (Otani et al 1991;Hogan et al 1994). In one method (Otani et al 1991), eight-cellstage embryos were collected in modified Whitten's (MW) medium by flushing the ampullae of the oviducts with MW medium under a dissecting microscope.…”

Section: Embryo Transfermentioning

confidence: 99%

“…Embryo transfer was performed utilizing well-established techniques (Otani et al 1991;Hogan et al 1994). In one method (Otani et al 1991), eight-cellstage embryos were collected in modified Whitten's (MW) medium by flushing the ampullae of the oviducts with MW medium under a dissecting microscope. The embryos were cultured in MW medium in an atmosphere of 5% O 2 /5% CO 2 /90% N 2 at 37∞C.…”

Section: Embryo Transfermentioning

confidence: 99%

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Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non‐obese diabetic mice

Kagohashi

Udagawa

Moriyama

et al. 2005

Congenital Anomalies

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Type 1 diabetes results from the destruction of pancreatic b-cells (insulitis). It is a multifactorial disease involving genetic and environmental factors, including the maternal environment. Viruses have also been implicated in the pathogenesis of human type 1 diabetes as well as in its model non-obese diabetic (NOD) mice during the perinatal period, as endogenous viruses and/or as infectious agents vertically transmitted from mothers. However, the role of virus as genetic or environmental factor and its interaction with other maternal factors remain unclear. In a series of experiments, we transplanted preimplantation-stage NOD embryos into the uterus of recipient Institute of Cancer Research (ICR) mice, which are without diabetic genetic predisposition, and NOD mice, which did not exhibit overt diabetes during the experiment, and designated offspring as NOD/ICR and NOD/NOD, respectively. We previously observed that NOD/ICR offspring developed insulitis significantly earlier than NOD/NOD offspring. To assess the role of viruses in the development of insulitis, we examined the appearance of viral particles and expression of retroviruses between NOD/ICR and NOD/NOD. NOD/ICR showed earlier expression of env region of the xenotropic type C retrovirus by polymerase chain reaction analysis than NOD/NOD, while the retrovirus-like particles were observed in the islet b-cells similarly in both groups by electron microscopy. Serum corticosterone level, which is suggested to enhance retroviral induction, was significantly higher in the ICR than in the NOD surrogate mothers. These findings suggest that the observed virus is endogenous and that maternal environmental factors, including hormone levels, affect the induction of endogenous viruses and cause the earlier onset of insulitis.

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Section: Discussionmentioning

confidence: 99%

Section: Embryo Transfermentioning

confidence: 99%

Section: Embryo Transfermentioning

confidence: 99%

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Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non‐obese diabetic mice

Kagohashi

Udagawa

Moriyama

et al. 2005

Congenital Anomalies

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“…We previously reported on the chromosomes of preimplantationstage NOD and ICR embryos cultured to transfer mutually between NOD and ICR mice (Tatewaki et al 1989a;Otani et al 1991). There was no significant difference among the ratios of chromosomal abnormalities, suggesting that developmental abnormality did not occur at least in chromosomal level during the preimplantation stage.…”

Section: Chromosome Analysismentioning

confidence: 93%

“…We have also investigated the diabetic environment and genetic factors as causal mechanisms in these developmental anomalies in the offspring from diabetic mothers (Tatewaki et al 1989a(Tatewaki et al ,b, 1991(Tatewaki et al , 1995Otani et al 1991), as well as in the pathogenesis of diabetes (Kagohashi et al 2005a,b). A high incidence in chromosomal abnormalities, especially numerical abnormalities, was found in the externally abnormal embryos of diabetic non-obese-diabetic (NOD) mice ).…”

Section: Introductionmentioning

confidence: 99%

Analysis of polyploid cells in mouse embryonic cells cultured under diabetic conditions

Tatewaki

Kagohashi

Otani

2006

Congenital Anomalies

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To clarify the cytogenetic effects of glucose and ketone bodies on the pathogenesis of diabetes-associated congenital anomalies, we cultured cells from gestation-day-8 ICR mouse embryos under the diabetic condition. Cells were cultured in the medium with glucose (300 mg/dL) plus DL-2-hydroxybutyric acid (32 mM) (G + B group), glucose alone (G group), or neither of them (C group) for 5 days. At the end of the culture, cells were analyzed for the chromosomes. After 3-4 days culture, when the living cells grew into a mono-layered sheet, cells floating in the medium were observed and showed morphological features of apoptosis. Ratio of the floating cells was significantly higher in the G + B group than in the G or C group (P < 0.05), suggesting the deleterious effect of glucose and ketone body. Polyploidy was observed in the cultured cells more frequently in the G + B group (64.1%) than in the G group (49.0%), which was higher than the C group (20.5%) (G + B vs G: P < 0.05, G vs C: P < 0.001). The higher ratio of the polyploidy, but not of the aneuploidy, in the G + B and G groups suggested the specific effect of glucose and ketone body for inducing polyploidy. These results suggest that diabetic condition causes polyploidy in cultured embryonic cells.

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Diabetes in Pregnancy

Dornhorst

2010

Textbook of Diabetes

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Diabetic environment and genetic predisposition as causes of congenital malformations in NOD mouse embryos

Cited by 24 publications

References 0 publications

Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non‐obese diabetic mice

Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non‐obese diabetic mice

Analysis of polyploid cells in mouse embryonic cells cultured under diabetic conditions

Diabetes in Pregnancy

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