ArticleMolecules and cells2024
ER stress and unfolded protein response (UPR) signaling modulate GLP-1 receptor signaling in the pancreatic islets.
Article in Molecules and cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- GLP-1 Receptor Agonists as Molecular Relievers of Lipotoxic Stress: From Pancreatic Beta-Cell Cholesterol Efflux to Systemic and Tissue-Specific Metabolic Protection.International journal of molecular sciences · 2026Review
- Article
- Distinctive molecular architectures of GActa pharmaceutica Sinica. B · 2026Article
- ERp46 mitigates lipotoxic ER stress to preserve GLUT2 expression and insulin secretion in β-cells.Biomedical reports · 2026Article
- Pharmacological chaperones mitigate noise-induced hearing loss by attenuating sustained PERK activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
- Pancreatic β-cell FFA2 deficiency suppresses multiple low dose streptozotocin induced diabetes in male mice.Communications biology · 2025Article
- Single-cell sequencing insights into the transcriptional landscape of cerebral cavernous malformations.Angiogenesis · 2025Review
- Brief guide to assays for measuring health parameters using Caenorhabditis elegans.Molecules and cells · 2025Review
- GLP-1 receptor agonists: exploration of transformation from metabolic regulation to multi-organ therapy.Frontiers in pharmacology · 2025Review
- Dipeptidyl peptidase 4 as an injury-responsive protein in the mouse sciatic nerve.Molecules and cells · 2024Article
- The emerging role of gut hormones.Molecules and cells · 2024Review
- Nitrogen-doped carbon quantum dot regulates cell proliferation and differentiation by endoplasmic reticulum stress.Animal cells and systems · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin is essential for maintaining normoglycemia and is predominantly secreted in response to glucose stimulation by β-cells. Incretin hormones, such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, also stimulate insulin secretion. However, as obesity and type 2 diabetes worsen, glucose-dependent insulinotropic polypeptide loses its insulinotropic efficacy, whereas GLP-1 receptor (GLP-1R) agonists continue to be effective owing to its signaling switch from Gs to Gq. Herein, we demonstrated that endoplasmic reticulum (ER) stress induced a transition from Gs to Gq in GLP-1R signaling in mouse islets. Intriguingly, chemical chaperones known to alleviate ER stress, such as 4-PBA and TUDCA, enforced GLP-1R's Gq utilization rather than reversing GLP-1R's signaling switch induced by ER stress or obese and diabetic conditions. In addition, the activation of X-box binding protein 1 (XBP1) or activating transcription factor 6 (ATF6), 2 key ER stress-associated signaling (unfolded protein response) factors, promoted Gs utilization in GLP-1R signaling, whereas Gq employment by ER stress was unaffected by XBP1 or ATF6 activation. Our study revealed that ER stress and its associated signaling events alter GLP-1R's signaling, which can be used in type 2 diabetes treatment.
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