Colour: Albino,
Genet. c.
Origin: Mutation causing diabetes mellitus in a closed colony of outbred Wistar rats at Bio-Breeding Labs, Ontario, Canada in 1974 (Chappel and Chappel 1983). To Worcester in 1977 where inbreeding began. Sublines of diabetic-prone and diabetic-resistant animals have been developed, and there are also subline differences in the incidence, age of onset, untreated survival time of diabetes, leucopenia and body weight gain which can be attributed to genetic factors (Kloting et al 1987). A detailed study of 24 inbred and two outbred lines of diabetes-prone and diabetes resistant BB rats using eight marker loci found substantial genetic variation among and some variation within some of the colonies. The 22 colonies which were apparently isogenic could be divided into four groups on the basis of the marker loci (Prins et al 1990).
Lifespan and spontaneous disease
Abrupt onset of insulin-dependent, ketosis-prone diabetes between 60 and 120 days of age. Animals exhibit lymphocyte insulinitis with virtually complete destruction of pancreatic beta cells; T cell lymphopenia; lymphocytic thyroiditis, and autoantibodies to smooth muscle, thyroid colloid, and gastric parietal cells. T cell lymphopenia is due largely to the absence of RT6+ peripheral T cell subset, including members of both helper/inducer and suppressor/cytotoxic antigenic phenotypes (Greiner et al 1986). Isolated, perfused kidneys from diabetic animals show higher basal renin release and kidney renin content than kidneys from nondiabetic controls. Renin-secretory response to beta-adrenergic stimulation impaired (Cohen et al 1986). About 32% of diabetic rats develop gastric erosions and ulcerations compared with only 10% of non-diabetic BB rats (Wright et al 1981). Further discussions of the characteristics of this model are given in Metabolism 32 no 7 suppl.1, (1983) and in Mordes et al (1987). Poly I:C accelerates the development of diabetes both in diabetes-prone and resistant substrains (Sobel et al 1992, Ewel et al 1992). The development of lymphocytic thyroiditis is not affected by iodine treatment according to Allen (1992), though Ebner et al (1992) found that it does have some affect. Epitope specificities of collagen-induced arthritis studied by Cremer et al (1992). A lymphopenic, nondiabetic substrain BB-DR has very low T-cell numbers, depressed B-lymphocyte numbers and a complete absence of peripheral CD8+ T cells characteristics of the susceptible BB strain (Joseph et al 1993). Transfusing of BB-DR thymocytes into nude rats transfers the autoimmune insulin-dependent diabetes mellitus (Whalen et al 1995). The percentage of animals getting diabetes by 200 days of age depends on the sex distribution within litters and the phenotype of the parents. A maximum liklihood model for predicting the incidence of diabetes each generation has been developed by Vogt and Kloting (1993). In-vitro study of perfused islets suggested that diabetes is due to a reduction on beta cell mass (Teruya et al 1993). Endothelin urinary excretion is increased in diabetic BB rats (Morabito et al 1994).
Drugs and chemicals
The sulfonylurea drug glipizide delays onset and decreases the incidence of diabetes (Hosszufalusi et al 1994).
Mordes J. P., Desemone J., and Rossini A. A. (1987) The BB rat. Diab. Metab. Rev. 3, 725-750.
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/19/2024 MGI 6.24 |
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