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Streptozotocin and alloxan-based selection improves toxin resistance of insulin-producing RINm cells

K O Bloch1, R Zemel, O V Bloch

  • 1Diabetes and Obesity Research Laboratory, Felsenstein Medical Research Center of Tel-Aviv University, Petah Tikva, Israel. pvardi@post.tau.ac.il

International Journal of Experimental Diabetes Research
|July 27, 2001
PubMed

Insights

Researchers developed a method to select insulin-producing RINm cells resistant to beta cell toxins like streptozotocin (STZ) and alloxan (AL). Selected cells showed enhanced toxin resistance and higher insulin production, suggesting GLUT-2 involvement.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Toxicology

Background:

  • Insulin-producing beta cells are vulnerable to toxins.
  • Developing methods to enhance beta cell resistance is crucial for understanding and treating diabetes.

Purpose of the Study:

  • To develop a method for selecting RINm cell subpopulations with increased resistance to beta cell toxins.
  • To investigate the role of GLUT-2 in cellular response to toxins.

Main Methods:

  • Repeated exposure of RINm cells to streptozotocin (STZ) and alloxan (AL).
  • Assessment of cell defense capacity using MTT colorimetric assay and [3H]-thymidine incorporation.
  • Western blot analysis to determine GLUT-2 expression levels.

Main Results:

  • Selected RINmS (streptozotocin-resistant) and RINmA (alloxan-resistant) cells exhibited higher resistance to STZ and AL compared to parental RINm cells.
  • No difference in hydrogen peroxide sensitivity was observed between selected and parental cells.
  • Selected cells (RINmS and RINmA) demonstrated higher insulin content and secretion.
  • Western blot analysis revealed lower GLUT-2 expression in RINmS and RINmA cells compared to parental RINm cells.

Conclusions:

  • Streptozotocin and alloxan treatment can select for RINm cell subpopulations with enhanced toxin resistance and improved insulin production.
  • The differential expression of GLUT-2 suggests its involvement in cellular mechanisms of toxin response.

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