ArticleBMC cell biology2013
Chronic glucolipotoxic conditions in pancreatic islets impair insulin secretion due to dysregulated calcium dynamics, glucose responsiveness and mitochondrial activity.
Article in BMC cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Modeling Adipokine and Insulin-Mediated Crosstalk Between Adipocytes and Beta Cells Using Flow-Enabled Microfluidics.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- miRNA-642a-3p protects β cells from glucolipotoxicity.Molecular therapy. Nucleic acids · 2025Article
- FGF-23 protects cell function and viability in murine pancreatic islets challenged by glucolipotoxicity.Pflugers Archiv : European journal of physiology · 2023Article
- Review
- Gut Metabolite Trimethylamine N-Oxide Protects INS-1 β-Cell and Rat Islet Function under Diabetic Glucolipotoxic Conditions.Biomolecules · 2021Article
- Beta-Cell Dysfunction Induced by Tacrolimus: A Way to Explain Type 2 Diabetes?International journal of molecular sciences · 2021Review
- Developmental Programming and Glucolipotoxicity: Insights on Beta Cell Inflammation and Diabetes.Metabolites · 2020Review
- Calpain inhibitor and ibudilast rescue β cell functions in a cellular model of Wolfram syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Recent Insights Into Mechanisms of β-Cell Lipo- and Glucolipotoxicity in Type 2 Diabetes.Journal of molecular biology · 2020Review
- Lipid Droplet Accumulation in Human Pancreatic Islets Is Dependent On Both Donor Age and Health.Diabetes · 2020Article
- Metabolic signatures suggest o-phosphocholine to UDP-N-acetylglucosamine ratio as a potential biomarker for high-glucose and/or palmitate exposure in pancreatic β-cells.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance.Oxidative medicine and cellular longevity · 2019Article
- Pepsin Egg White Hydrolysate Improves Glucose Metabolism Complications Related to Metabolic Syndrome in Zucker Fatty Rats.Nutrients · 2018Article
- Energy depletion and not ROS formation is a crucial step of glucolipotoxicity (GLTx) in pancreatic beta cells.Pflugers Archiv : European journal of physiology · 2018Article
- Chronic Exposure of Human Endothelial Progenitor Cells to Diabetic Condition Abolished the Regulated Kinetics Activity of Exosomes.Iranian journal of pharmaceutical research : IJPR · 2018Article
- Inhibition of cholinergic potentiation of insulin secretion from pancreatic islets by chronic elevation of glucose and fatty acids: Protection by casein kinase 2 inhibitor.Molecular metabolism · 2017Article
- Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity.Aging and disease · 2016Review
- Accumulation of 3-hydroxytetradecenoic acid: Cause or corollary of glucolipotoxic impairment of pancreatic β-cell bioenergetics?Molecular metabolism · 2015Article
- Protein-Binding Function of RNA-Dependent Protein Kinase Promotes Proliferation through TRAF2/RIP1/NF-κB/c-Myc Pathway in Pancreatic β cells.Molecular medicine (Cambridge, Mass.) · 2015Article
- A novel GPR40 agonist, CNX-011-67, suppresses glucagon secretion in pancreatic islets under chronic glucolipotoxic conditions in vitro.BMC research notes · 2014Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the progression towards diabetes, glucolipotoxicity is one of the main causes of pancreatic beta cell pathology. The aim of this study was to examine the in vitro effects of chronic glucolipotoxic conditions on cellular responses in pancreatic islets, including glucose and fat metabolism, Calcium mobilization, insulin secretion and insulin content.
resultsExposure of islets to chronic glucolipotoxic conditions decreased glucose stimulated insulin secretion in vitro. Reduced protein levels of Glut2/slc2a2, and decreased glucokinase and pyruvate carboxylase mRNA levels indicated a significant lowering in glucose sensing. Concomitantly, both fatty acid uptake and triglyceride accumulation increased significantly while fatty acid oxidation decreased. This general suppression in glucose metabolism correlated well with a decrease in mitochondrial number and activity, reduction in cellular ATP content and dampening of the TCA cycle. Further, we also observed a decrease in IP3 levels and lower Calcium mobilization in response to glucose. Importantly, chronic glucolipotoxic conditions in vitro decreased insulin gene expression, insulin content, insulin granule docking (to the plasma membrane) and insulin secretion.
conclusionsOur results present an integrated view of the effects of chronic glucolipotoxic conditions on known and novel signaling events, in vitro, that results in reduced glucose responsiveness and insulin secretion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.