ArticleInternational journal of molecular sciences2023
Modulation of Unfolded Protein Response Restores Survival and Function of β-Cells Exposed to the Endocrine Disruptor Bisphenol A.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Vitamin E fails to prevent bisphenol S induced testicular damage in diabetic rats.Scientific reports · 2026Article
- Endocrine-disrupting chemical exposure during differentiation alters the proliferation-maturation balance in stem-cell islets.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Chronic adulthood exposure to bisphenol A causes behavioral changes via suppressing dopamine transporter trafficking.Scientific reports · 2025Article
- Molecular profiling of NOD mouse islets reveals a novel regulator of insulitis onset.Scientific reports · 2024Article
- Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Diabetes is a metabolic disease that currently affects nearly half a billion people worldwide. β-cells dysfunction is one of the main causes of diabetes. Exposure to endocrine-disrupting chemicals is correlated with increased diabetes incidence. We hypothesized that treatment with bisphenol A (BPA) induces endoplasmic reticulum (ER) stress that activates the unfolded protein response (UPR), leading to impaired function of the β-cells, which over time, can cause diabetes. In this study, we aimed to evaluate UPR pathways activation under BPA treatment in β-cells and possible recovery of ER homeostasis. MIN6 cells (mouse insulinoma cell line) and isolated pancreatic islets from NOR (non-obese diabetes resistant) mice were treated with BPA. We analyzed the impact of BPA on β-cell viability, the architecture of the early secretory pathway, the synthesis and processing of insulin and the activation of UPR sensors and effectors. We found that the addition of the chemical chaperone TUDCA rescues the deleterious effects of BPA, resulting in improved viability, morphology and function of the β-cells. In conclusion, we propose that modulators of UPR can be used as therapeutic interventions targeted towards regaining β-cells homeostasis.
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Registered trials
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