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Related Experiment Video

Updated: Jun 12, 2026

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

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Published on: May 2, 2025

Insulin increases H2O2-induced pancreatic beta cell death.

S R Sampson¹, E Bucris, M Horovitz-Fried

¹Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel. ssampson@013.net

Apoptosis : an International Journal on Programmed Cell Death

|June 15, 2010

Summary

High insulin levels may harm pancreatic beta cells, increasing cell death. This study found insulin exacerbates hydrogen peroxide-induced cell death, potentially impacting diabetes management.

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Area of Science:

Endocrinology
Cell Biology
Diabetes Research

Background:

Insulin resistance necessitates higher insulin levels to maintain glucose homeostasis.
The impact of elevated insulin on pancreatic beta (β) cell survival remains largely unknown.

Purpose of the Study:

To investigate whether insulin influences the survival of pancreatic β cells.
To determine if insulin exacerbates apoptosis in pancreatic β cells under oxidative stress.

Main Methods:

Utilized pancreatic β-cell lines (RINm, RINm5F, Min-6).
Induced cell death using hydrogen peroxide (H₂O₂).
Assessed cell death via LDH levels, viability assays, propidium iodide staining, FACS analysis, mitochondrial membrane potential (JC-1), cleaved caspase-3, and caspase activity.

Main Results:

Hydrogen peroxide (H₂O₂) increased β-cell death; insulin amplified this effect.
Insulin alone caused a minor increase in cell death.
Inhibition of caspase-3 partially blocked insulin's effect on H₂O₂-induced cell death.
Insulin elevated reactive oxygen species (ROS) production and potentiated H₂O₂ effects, independent of insulin receptor (IR) signaling.

Conclusions:

Elevated insulin levels may worsen β-cell death induced by oxidative stress.
Insulin's detrimental effects on β-cell survival might be mediated by ROS production.
Findings suggest a potential mechanism contributing to β-cell dysfunction in conditions of hyperinsulinemia.