Pancreatic Endocrine Toxicity | InSphero

Assess drug-induced beta-cell injury in long-lived, robust 3D islet models

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 Microtissues enable studies to determine the effect of prolonged drug exposure on islet viability and functionality.

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  • Seino & Bell, 2008, Pancreatic Beta Cell in Health and Disease, Springer
  • Kitamura, 2013, Nature Reviews Endocrinology
Toxicity mechanism Cellular indicator
  • ATP-content
β-cell function/toxicity
  • Insulin content
  • Insulin secretion (chronic and basal)
  • Glucose-stimulated Insulin Secretion (GSIS)

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Brochure: Human Islet Microtissues


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