Use of Streptozotocin in Rodent Models of Islet Transplantation.

@article{King2020UseOS,
  title={Use of Streptozotocin in Rodent Models of Islet Transplantation.},
  author={Aileen J.F. King and Elisabet Estil les and Eduard Montanya},
  journal={Methods in molecular biology},
  year={2020},
  volume={2128},
  pages={
          135-147
        }
}
Streptozotocin (STZ) selectively destroys beta cells and is widely used to induce experimental diabetes in rodents. Rodent beta cells are very sensitive to the toxic effects of STZ, while human beta cells are highly resistant to STZ. Taking advantage of this characteristic, here, we describe two protocols for the induction of STZ-diabetes. In the first model, hyperglycemia is induced prior to islet transplantation, whereas in the second model, STZ is injected after islet transplantation. The… 
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References

SHOWING 1-7 OF 7 REFERENCES
A Model for Human Islet Transplantation to Immunodeficient Streptozotocin-Induced Diabetic Mice
TLDR
A new, more convenient and cost-saving model for human islet transplantation to STZ-diabetic recipients in which STZ is injected after islet transplanted islets is provided.
Human β Cells Are Exceedingly Resistant to Streptozotocin in Vivo.
Streptozotocin (STZ) causes β cell death in rodents via the mechanism of DNA damage precipitating poly(ADP-ribose) synthetase activation followed by lethal nicotinamide adenine dinucleotide
The streptozotocin-induced diabetic nude mouse model: differences between animals from different sources.
TLDR
Naked male mice from various sources are evaluated for their sensitivity to a single high dose of streptozotocin (STZ), a compound that has a preferential toxicity toward pancreatic β cells, and both TAC and JAX mice were more sensitive to STZ, as evidenced by faster development of diabetes and greater need for insulin.
Optimal Insulin Treatment in Syngeneic Islet Transplantation
TLDR
The beneficial effect of insulin-induced normoglycemia on transplanted islets was maximal when insulin treatment was maintained the initial 14 days after transplantation, indicating that impaired glucose tolerance was not due to reduced beta cell mass.
Improved outcome of islet transplantation in insulin-treated diabetic mice: effects on beta-cell mass and function
TLDR
Islets transplanted to insulin-treated mice showed better beta-cell function, preserved insulin content, and were able to increase their beta- cell mass to meet an increased functional demand.
Improvement in Islet Yield from Obese Donors for Human Islet Transplants
TLDR
Pancreases from both overweight (BMI ≥26 but <30) and obese cadaver donors are suitable for islet isolation and transplantations and their use could increase the size of the islet donor pool.
Beta cell mass and growth after syngeneic islet cell transplantation in normal and streptozocin diabetic C57BL/6 mice.
TLDR
With a successful islet transplant, in diabetic mice beta cell replication and mass remain constant, in contrast, when insufficient islet tissue is transplanted an initial increase in Beta cell replication can not compensate for a decline in beta cell mass.