ArticleDiabetologia2007
Increasing uncoupling protein-2 in pancreatic beta cells does not alter glucose-induced insulin secretion but decreases production of reactive oxygen species.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 73 citations in OpenAlex.
- Mitochondrial uncoupling protein 2: a central player in pancreatic disease pathophysiology.Molecular medicine (Cambridge, Mass.) · 2024Review
- UCP2 as a Cancer Target through Energy Metabolism and Oxidative Stress Control.International journal of molecular sciences · 2022Review
- Uncoupling protein 2 and aldolase B impact insulin release by modulating mitochondrial function and CaiScience · 2022Article
- Pancreatic Islets Exhibit Dysregulated Adaptation of Insulin Secretion after Chronic Epinephrine Exposure.Current issues in molecular biology · 2021Article
- EGCG Upregulates UCPDrug design, development and therapy · 2020Article
- Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.Antioxidants & redox signaling · 2018Review
- Upregulation of UCP2 in beta-cells confers partial protection against both oxidative stress and glucotoxicity.Redox biology · 2017Article
- The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus.Antioxidants & redox signaling · 2017Review
- H₂O₂-Activated Mitochondrial Phospholipase iPLA₂γ Prevents Lipotoxic Oxidative Stress in Synergy with UCP2, Amplifies Signaling via G-Protein-Coupled Receptor GPR40, and Regulates Insulin Secretion in Pancreatic β-Cells.Antioxidants & redox signaling · 2015Article
- When less is more: hormesis against stress and disease.Microbial cell (Graz, Austria) · 2014Review
- UCP2, a mitochondrial protein regulated at multiple levels.Cellular and molecular life sciences : CMLS · 2014Review
- Overlap of Doxycycline Fluorescence with that of the Redox-Sensitive Intracellular Reporter roGFP.Journal of fluorescence · 2014Article
- Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?Oxidative medicine and cellular longevity · 2012Review
- Redox homeostasis in pancreatic β cells.Oxidative medicine and cellular longevity · 2012Review
- Resveratrol potentiates glucose-stimulated insulin secretion in INS-1E beta-cells and human islets through a SIRT1-dependent mechanism.The Journal of biological chemistry · 2011Article
- Oxidative stress and beta-cell dysfunction.Pflugers Archiv : European journal of physiology · 2010Review
- Article
- Leucine metabolism in regulation of insulin secretion from pancreatic beta cells.Nutrition reviews · 2010Review
- Glucolipotoxicity of the pancreatic beta cell.Biochimica et biophysica acta · 2010Review
- Transient oxidative stress damages mitochondrial machinery inducing persistent beta-cell dysfunction.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisLevels of uncoupling protein-2 (UCP2) are regulated in the pancreatic beta cells and an increase in the protein level has been associated with mitochondrial uncoupling and alteration in glucose-stimulated insulin secretion. However, it is not clear whether an increase in uncoupling protein-2 per se induces mitochondrial uncoupling and affects ATP generation and insulin secretion. MATERIALS AND
methodsTransgenic mice with beta cell-specific overexpression of the human UCP2 gene and INS-1 cells with doxycycline-inducible overproduction of the protein were generated and the consequences of increased levels of UCP2 on glucose-induced insulin secretion and on parameters reflecting mitochondrial uncoupling were determined.
resultsIn transgenic mice, an increase in beta cell UCP2 protein concentration did not significantly modify plasma glucose and insulin levels. Glucose-induced insulin secretion and elevation in the ATP/ADP ratio were unaltered by an increase in UCP2 level. In INS-1 cells, a similar increase in UCP2 level did not modify glucose-induced insulin secretion, cytosolic ATP and ATP/ADP ratio, or glucose oxidation. Increased levels of UCP2 did not modify the mitochondrial membrane potential and oxygen consumption. Increased UCP2 levels decreased cytokine-induced production of reactive oxygen species. CONCLUSION/
interpretationThe results obtained in transgenic mice and in the beta cell line do not support the hypothesis that an increase in UCP2 protein per se uncouples the mitochondria and decreases glucose-induced insulin secretion. In contrast, the observation that increased UCP2 levels decrease cytokine-induced production of reactive oxygen species indicates a potential protective effect of the protein on beta cells, as observed in other cell types.
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