ArticleInternational journal of endocrinology2026
Gomisin N Improves Insulin Secretion by Alleviating Endoplasmic Reticulum and Oxidative Stress in Pancreatic Beta Cells.
Article in International journal of endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Gomisin N Improves Insulin Secretion by Alleviating Endoplasmic Reticulum and Oxidative Stress in Pancreatic Beta Cells.International journal of endocrinology · 2026Article
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Authors and funding
2 authors.
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Abstract
This study investigated the effects of gomisin N (25 μM) using a cyclopiazonic acid (CPA, 50 μM)-induced injury model of MIN6 pancreatic beta-cells. The results demonstrated that gomisin N effectively reduced the expression of endoplasmic reticulum (ER) stress markers that were increased by CPA. Furthermore, gomisin N treatment improved insulin secretion from MIN6 cells, which had been reduced by CPA. These findings suggest that alleviation of ER stress and oxidative stress ultimately supports the correct folding and maturation of insulin precursors and enhances beta-cell viability, leading to functional normalization. Gomisin N exhibited antioxidant effects by significantly reducing reactive oxygen species (ROS) levels that were increased by CPA. Given that ER stress and oxidative stress are closely linked and cooperatively drive cellular damage, the dual stress-relieving properties of gomisin N are critical for beta-cell protection. By alleviating ER stress and reducing oxidative stress, gomisin N acts to protect and restore insulin secretory function in beta-cells. Therefore, gomisin N could play a beneficial role in protecting and improving pancreatic beta-cell function, particularly under stress conditions.
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