Streptozotocin‐Induced Diabetic Models in Mice and Rats

Streptozotocin was initially isolated from Streptomyces achromogenes in 1960, with its diabetogenic properties not described until 1963

Brian L. Furman

2015

Scholarcy highlights

  • Streptozotocin was initially isolated from Streptomyces achromogenes in 1960, with its diabetogenic properties not described until 1963
  • This action was characterized by previous research based on earlier work showing that the diabetogenic effects are due to selective destruction of pancreatic islet β-cells
  • As a result of this action, the animals experience insulin deficiency, hyperglycemia, polydipsia, and polyuria, all of which are characteristic of human type 1 diabetes mellitus (T1DM;
  • If the diabetic animals are for assessing early-stage mechanisms of T1DM or for screening compounds for treatment of early-stage diabetes, the models are validated for further study when hyperglycemia is established in the STZ-injected rats
  • Low-dose STZ-induced diabetic mouse models may more closely resemble human T1DM than models in which hyperglycemia is induced by a single large dose of the toxin, because of the association of hyperglycemia with lymphocytic infiltration of the pancreatic islets, marked β-cell apoptosis, insulitis, and insulin deficiency
  • As there is evidence for the contribution of autoimmunity in this model, it is much more suitable for studying the underlying pathogenesis of T1D than the high-dose STZ models where direct, toxin-induced necrosis of the β-cell is the predominant mode of cell death
  • Rats rendered diabetic using the STZ protocol develop nephropathy, making this a useful model for studying potential treatments for this condition (e.g.,

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