Amyloid beta (Aβ) peptides, known for their involvement in neurodegenerative diseases like Alzheimer's, have recently been recognized as significant contributors to metabolic disorders, including type 2 diabetes. This study examined the effects of Aβ40 and Aβ42 peptides on cell viability and glucose-stimulated insulin secretion in rat insulinoma (INS-1) cells. Aβ40 treatment demonstrated no significant toxicity at lower concentrations; however, it did reduce cell viability at higher concentrations and with prolonged exposure. Conversely, Aβ42 exhibited notable cytotoxicity even at lower concentrations within 24 hours. The combined treatment of Aβ40 and Aβ42 at a 10:1 ratio further accelerated the decline in cell viability, indicating a synergistic toxic effect. Importantly, Aβ40/42 treatment did not impair glucose-stimulated insulin secretion in INS-1 cells under the conditions tested. These findings suggest that Aβ peptides may contribute to β-cell loss in type 2 diabetes through their cytotoxic effects, although the direct impact on insulin secretion requires further study. Nutritional interventions aimed at reducing Aβ aggregation and associated oxidative stress could offer promising strategies to protect β-cell viability, warranting further research to clarify the underlying mechanisms of such dietary modulation.

Abstract
Introduction
Methods
    1. Cell
    2. Cell viability
    3. Annexin V-PE staining
    4. Glucose stimulated insulin secretion (GSIS)
    5. Statistical analysis
Results and Discussion
    1. Cell viability on Aβ40 and Aβ42-treated INS-1 cells
    2. GSIS on Aβ40/Aβ42-treated INS-1 cells
Conclusion
Acknowledgements
References

• Eun-Young Park(Professor, College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Mokpo 58645, Korea)
• Yoon Sin Oh(Professor, Dept. of Food and Nutrition, Eulji University, Seongnam 13135, Korea) Corresponding author