Pancreatic Endocrine Toxicity: Assess drug-induced beta-cell injury in long-lived, robust 3D islet models
Pancreatic Endocrine Toxicity: Decreased β-cell mass is an important factor in the pathogenesis of type 2 diabetes and thus raises a concern regarding the application of drugs potentially harmful to the remaining beta cells (1).
Several stimuli, such as increased oxidative stress, ER-stress, hypoxia and cytokine induction, are known to cause beta-cell apoptosis or de-differentiation, and have been shown to impair beta-cell functionality (2).
Drugs stimulating these effects might harm beta-cell functionality. In addition, drugs designed to target beta-cells directly might cause impairment of their viability and functionality after long-term treatment.
With the robust functionality over more than 28 days in culture, 3D InSight™ Islet Organoids enable pancreatic endocrine toxicity studies to determine the effect of prolonged drug exposure on islet viability and functionality.
Pancreatic Endocrine Toxicity: Assess drug-induced beta-cell injury in long-lived, robust 3D islet models
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References
- Seino & Bell, 2008, Pancreatic Beta Cell in Health and Disease, Springer.
- Kitamura, 2013, Nature Reviews Endocrinology
Toxicity mechanism | Cellular indicator |
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Cytotoxicity |
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β-cell function/toxicity |
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