Present address: K. Moriyama, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan.
Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non-obese diabetic mice
Version of Record online: 30 AUG 2005
Volume 45, Issue 3, pages 80–84, September 2005
How to Cite
Kagohashi, Y., Udagawa, J., Moriyama, K. and Otani, H. (2005), Maternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non-obese diabetic mice. Congenital Anomalies, 45: 80–84. doi: 10.1111/j.1741-4520.2005.00071.x
- Issue online: 30 AUG 2005
- Version of Record online: 30 AUG 2005
- Received December 15, 2004; revised and accepted May 11, 2005.
- embryo transfer;
- endogenous virus;
- maternal environment;
- non-obese diabetic mice
ABSTRACT 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.