title: A morphological study on the reproductive organs as a possible cause of developmental abnormalities in diabetic NOD mice.
abstract: The reproductive organs in non-obese diabetic (NOD) mice were histopathologically studied, in order to elucidate the relationships between developmental abnormalities, such as diminished rates of implantation and viable embryos, and structural changes in the reproductive organs. NOD mice with (NOD-DM) and without (NOD-N) diabetes mellitus and ICR mice were compared. The severity of histopathological changes in the pancreas and in the liver were used as parameters which indicated the severity of diabetes itself and of the secondary metabolic disorder. NOD-DM mice exhibited uterine weight loss, accumulation of lipids in luminal and glandular epithelium, atrophies of the endometrium and myometrium and a decrease in the number of muscle cell layers. They also showed a high concentration of lipid droplets in ovarian granulosa cells, atretic follicles and atrophy and lack of lipids in ovarian stroma cells. The severity of these structural changes in the reproductive organs corresponded to those of the changes in the pancreas and the liver. The structural alterations in the ovary suggested disorder in oocyte maturation. The structural changes in the uterus appeared to be related to the decrease in the ratios of implantation and of viable embryos at post-implantation stage. The present studies suggest that the impaired structural environment together with the metabolic environment caused the abnormal development seen, for example, in the oocyte maturation, and at the implantation and post-implantation stage of diabetic mice. It also caused alterations in their hormonal environment.
authors.affiliation: Department of Biology, Shimane Medical University, Izumo, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Tatewaki
authors.forename: H
authors.initials: H
authors.lastname: Otani
authors.forename: O
authors.initials: O
authors.lastname: Tanaka
authors.forename: J
authors.initials: J
authors.lastname: Kitada
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000473:pathology*; D005187:Fallopian Tubes / Q000473:pathology* / Q000648:ultrastructure; D005260:Female; D007668:Kidney / Q000473:pathology / Q000648:ultrastructure; D008099:Liver / Q000473:pathology / Q000648:ultrastructure; D051379:Mice; D008813:Mice, Inbred ICR; D016688:Mice, Inbred NOD; D009215:Myometrium / Q000473:pathology / Q000648:ultrastructure; D006080:Ovarian Follicle / Q000473:pathology / Q000648:ultrastructure; D010053:Ovary / Q000473:pathology* / Q000648:ultrastructure; D010179:Pancreas / Q000473:pathology / Q000648:ultrastructure; D014599:Uterus / Q000473:pathology* / Q000648:ultrastructure