ArticleDiabetologia2007
Acute nutrient regulation of the unfolded protein response and integrated stress response in cultured rat pancreatic islets.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 152 citations in OpenAlex.
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- A review of autophagy in the pancreas: normal physiology and pathophysiology.Autophagy reports · 2026Review
- Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications.International journal of molecular sciences · 2025Review
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- An adipocentric perspective of pancreatic lipotoxicity in diabetes pathogenesis.The Journal of endocrinology · 2024Review
- Dysfunctions, molecular mechanisms, and therapeutic strategies of pancreatic β-cells in diabetes.Apoptosis : an international journal on programmed cell death · 2023Review
- A highly sensitive strategy for monitoring real-time proliferation of targeted cell types in vivo.Nature communications · 2023Article
- Beta cell endoplasmic reticulum stress drives diabetes in the KINGS mouse without causing mass beta cell loss.Diabetic medicine : a journal of the British Diabetic Association · 2022Review
- Destabilization of β Cell FIT2 by saturated fatty acids alter lipid droplet numbers and contribute to ER stress and diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Ischemic brain injury in diabetes and endoplasmic reticulum stress.Neurochemistry international · 2022Review
- Biosynthetic Activity Differs Between Islet Cell Types and in Beta Cells Is Modulated by Glucose and Not by Secretion.Endocrinology · 2021Article
- Androgens impair β-cell function in a mouse model of polycystic ovary syndrome by activating endoplasmic reticulum stress.Endocrine connections · 2021Article
- Pathological β-Cell Endoplasmic Reticulum Stress in Type 2 Diabetes: Current Evidence.Frontiers in endocrinology · 2021Review
- Potential Roles of Endoplasmic Reticulum Stress and Cellular Proteins Implicated in Diabesity.Oxidative medicine and cellular longevity · 2021Review
- Developmental Programming and Glucolipotoxicity: Insights on Beta Cell Inflammation and Diabetes.Metabolites · 2020Review
- Pancreatic β-cells in type 1 and type 2 diabetes mellitus: different pathways to failure.Nature reviews. Endocrinology · 2020Review
- Mitochondrial pyruvate and fatty acid flux modulate MICU1-dependent control of MCU activity.Science signaling · 2020Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisInadequate chaperone function relative to client protein load in the endoplasmic reticulum triggers an adaptive unfolded protein response (UPR), including the integrated stress response (ISR), the latter being also activated by other types of stresses. It is well established that pancreatic beta cells, which synthesise and secrete insulin upon nutrient stimulation, are markedly affected by pathological disruption or excessive activation of the UPR. However, whether and how physiological nutrient stimulation affects the beta cell UPR has been little investigated. MATERIALS AND
methodsWe compared the effects of increasing glucose concentrations and of endoplasmic reticulum Ca(2+) emptying with thapsigargin on the UPR (X-box binding protein [Xbp1] mRNA splicing and XBP1/activating transcription factor [ATF] 6-target gene expression) and ISR (eukaryotic translation initiation factor 2A phosphorylation, ATF4 protein levels and target gene expression) in isolated rat islets.
resultsThapsigargin strongly increased both UPR and ISR. In comparison, glucose moderately increased the UPR between 5 and 30 mmol/l, but exerted complex effects on the ISR as follows: (1) marked reduction between 2 and 10 mmol/l; (2) moderate increase parallel to the UPR between 10 and 30 mmol/l. These glucose effects occurred within 2 h, were mimicked by other metabolic substrates, but were independent of changes in Ca(2+) influx or insulin secretion. Remarkably, attenuating the glucose stimulation of protein synthesis with a low concentration of cycloheximide prevented UPR activation but not ISR reduction by high glucose. CONCLUSIONS/
interpretationNutrient stimulation acutely activates rat islet UPR in a manner dependent on protein synthesis, while exerting complex effects on the ISR. These effects may contribute to nutrient-induced maintenance of the beta cell phenotype.
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