Abstract
Multiple treatment with low doses of streptozotocin induces in mice an experimental autoimmune diabetes characterized by hyperglycemia and lymphocytic infiltrations of pancreatic islets. We have studied the genetic control of the disease. Low-dose streptozotocin treatment was performed in mice of H-2 congenic strains on B10, C3H, or A background. Blood glucose concentrations were followed up to 100 days. Among the various B10 and C3H strains, significant differences in the development of diabetes (hyperglycemia) are noted demonstrating that genes within the H-2 complex influence the susceptibility to the diabetogenic effect of low-dose streptozotocin treatment. The congenic mouse strains on A background did not differ significantly in the diabetic response to streptozotocin. The analysis of B10 recombinant strains shows that genes coding for susceptibility are located in the centromeric (left) side of the H-2 complex. Evidence for an additional role of non-H-2 genes is given by comparison of mouse strains carrying the same H-2 haplotype on different genetic background genomes: B10.S (H-2s), B10.S(7R) (H-2t2), and C3H.SW (H-2b) are resistant to the diabetic effect of low-dose streptozotocin treatment, whereas A.SW (H-2s), A.TH (H-2t2) and B10 (H-2b) are susceptible to diabetes development.
Published Version
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