Related Experiment Video
Updated: Aug 10, 2026

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
Gomisin N Improves Insulin Secretion by Alleviating Endoplasmic Reticulum and Oxidative Stress in Pancreatic Beta
Joo Young Lee1,2, Chong Kun Cheon1,2
1Department of Pediatrics, Pusan National University School of Medicine, Pusan National University Children's Hospital, Yangsan 50612, Gyeongsangnam-do, South Korea, pnuyh.or.kr.
None:
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.
Related Concept Videos
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
Insulin and C-peptide are co-secreted in...
Insulin Secretory Vesicles
Dipeptidyl Peptidase 4 Inhibitors
Insulin: Biosynthesis, Chemistry, and Preparation
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Oral Hypoglycemic Agents: Glinides
