ArticlePloS one2015
Diabetes Alters the Expression and Translocation of the Insulin-Sensitive Glucose Transporters 4 and 8 in the Atria.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 75 citations in OpenAlex.
- Metabolism fine tuning and cardiokines secretion represent adaptative responses of the heart to High Fat and High Sugar Diets in flies.PLoS genetics · 2026Article
- Effect of SGLT2 Inhibitors on Atrial Fibrillation in Patients With Type 2 Diabetes With Dilated Cardiomyopathy: A Cohort Study.Cardiovascular therapeutics · 2026Article
- Altered Pulmonary Glucose Transport Is Restored by Metformin Treatment in an Obese Type 2 Diabetic Animal Model.Metabolites · 2025Article
- Cellular and Molecular Pathways in Diabetes-Associated Heart Failure: Emerging Mechanistic Insights and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Advances in myocardial energy metabolism: metabolic remodelling in heart failure and beyond.Cardiovascular research · 2024Review
- Unraveling the Roles of HIF-1, HO-1, GLUT-1 and GLUT-4 in Myocardial Protection.International journal of drug discovery and pharmacology · 2024Article
- Diabetes Causes Significant Alterations in Pulmonary Glucose Transporter Expression.Metabolites · 2024Article
- Opisthorchis viverrini excretory-secretory products suppress GLUT8 of cholangiocytes.Parasitology research · 2024Article
- Anti-Diabetic Activity of Glycyrrhetinic Acid Derivatives FC-114 and FC-122: Scale-Up, In Silico, In Vitro, and In Vivo Studies.International journal of molecular sciences · 2023Article
- Relevance of Sugar Transport across the Cell Membrane.International journal of molecular sciences · 2023Review
- Understanding the Mechanism Underlie the Antidiabetic Activity of Oleuropein UsingReports of biochemistry & molecular biology · 2022Article
- Placental expression of glucose transporters GLUT-1, GLUT-3, GLUT-8 and GLUT-12 in pregnancies complicated by gestational and type 1 diabetes mellitus.Journal of diabetes investigation · 2022Article
- An appraisal of the current status of inhibition of glucose transporters as an emerging antineoplastic approach: Promising potential of new pan-GLUT inhibitors.Frontiers in pharmacology · 2022Review
- Molecular and cellular mechanisms in diabetic heart failure: Potential therapeutic targets.Frontiers in endocrinology · 2022Review
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- Anti-inflammatory role of Gpnmb in adipose tissue of mice.Scientific reports · 2021Article
- Insulin signaling in the heart.American journal of physiology. Endocrinology and metabolism · 2021Review
- Current understanding of glucose transporter 4 expression and functional mechanisms.World journal of biological chemistry · 2020Review
- Disruption of energy utilization in diabetic cardiomyopathy; a mini review.Current opinion in pharmacology · 2020Review
- Glucose transporters in cardiovascular system in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although diabetes has been identified as a major risk factor for atrial fibrillation, little is known about glucose metabolism in the healthy and diabetic atria. Glucose transport into the cell, the rate-limiting step of glucose utilization, is regulated by the Glucose Transporters (GLUTs). Although GLUT4 is the major isoform in the heart, GLUT8 has recently emerged as a novel cardiac isoform. We hypothesized that GLUT-4 and -8 translocation to the atrial cell surface will be regulated by insulin and impaired during insulin-dependent diabetes. GLUT protein content was measured by Western blotting in healthy cardiac myocytes and type 1 (streptozotocin-induced, T1Dx) diabetic rodents. Active cell surface GLUT content was measured using a biotinylated photolabeled assay in the perfused heart. In the healthy atria, insulin stimulation increased both GLUT-4 and -8 translocation to the cell surface (by 100% and 240%, respectively, P<0.05). Upon insulin stimulation, we reported an increase in Akt (Th308 and s473 sites) and AS160 phosphorylation, which was positively (P<0.05) correlated with GLUT4 protein content in the healthy atria. During diabetes, active cell surface GLUT-4 and -8 content was downregulated in the atria (by 70% and 90%, respectively, P<0.05). Akt and AS160 phosphorylation was not impaired in the diabetic atria, suggesting the presence of an intact insulin signaling pathway. This was confirmed by the rescued translocation of GLUT-4 and -8 to the atrial cell surface upon insulin stimulation in the atria of type 1 diabetic subjects. In conclusion, our data suggest that: 1) both GLUT-4 and -8 are insulin-sensitive in the healthy atria through an Akt/AS160 dependent pathway; 2) GLUT-4 and -8 trafficking is impaired in the diabetic atria and rescued by insulin treatment. Alterations in atrial glucose transport may induce perturbations in energy production, which may provide a metabolic substrate for atrial fibrillation during diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.