ArticleThe Journal of clinical investigation1999
Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers.
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Who cites it
174 citing papers in PubMed, 360 citations in OpenAlex.
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- Metabolic Remodeling Induced by Exercise: Emerging Mechanisms for Myocardial Protection in Cardiovascular Disease.Journal of cardiovascular translational research · 2026Review
- Ketone Catabolism Is Essential for Maintaining Normal Heart Function During Aging.Journal of the American Heart Association · 2025Article
- Deletion of PTP1B in cardiomyocytes alters cardiac metabolic signaling to protect against cardiomyopathy induced by a high-fat diet.Science signaling · 2025Article
- Novel insights into post-myocardial infarction cardiac remodeling through algorithmic detection of cell-type composition shifts.PLoS genetics · 2025Article
- Protein O-GlcNAcylation and hexokinase mitochondrial dissociation drive heart failure with preserved ejection fraction.Cell metabolism · 2025Article
- An NRF2/β3-Adrenoreceptor Axis Drives a Sustained Antioxidant and Metabolic Rewiring Through the Pentose-Phosphate Pathway to Alleviate Cardiac Stress.Circulation · 2025Article
- Cre recombinase affects calcium dynamics already in young mice.Frontiers in pharmacology · 2025Article
- Cardiomyocyte-Specific FoxO1 Knockout Mice as Tools to Assess Cardiac Hypertrophy and Key Experimental Considerations Using Cre-loxP.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Regulation of injury-induced skeletal myofiber regeneration by glucose transporter 4 (GLUT4).Skeletal muscle · 2024Article
- Article
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Nature immunology · 2024Article
- AS160 is a lipid-responsive regulator of cardiac CaNature communications · 2024Article
- Sex-specific regulation of the cardiac transcriptome by the protein phosphatase 2A regulatory subunit B55α.npj metabolic health and disease · 2024Article
- Comparative analysis of two independent Myh6-Cre transgenic mouse lines.Journal of molecular and cellular cardiology plus · 2024Article
- Insulin-Heart Axis: Bridging Physiology to Insulin Resistance.International journal of molecular sciences · 2024Review
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Research square · 2024Article
- Cardiac monoamine oxidase-A inhibition protects against catecholamine-induced ventricular arrhythmias via enhanced diastolic calcium control.Cardiovascular research · 2024Article
- The glucocorticoid receptor acts locally to protect dystrophic muscle and heart during disease.Disease models & mechanisms · 2024Article
114 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Glucose enters the heart via GLUT1 and GLUT4 glucose transporters. GLUT4-deficient mice develop striking cardiac hypertrophy and die prematurely. Whether their cardiac changes are caused primarily by GLUT4 deficiency in cardiomyocytes or by metabolic changes resulting from the absence of GLUT4 in skeletal muscle and adipose tissue is unclear. To determine the role of GLUT4 in the heart we used cre-loxP recombination to generate G4H(-/-) mice in which GLUT4 expression is abolished in the heart but is present in skeletal muscle and adipose tissue. Life span and serum concentrations of insulin, glucose, FFAs, lactate, and beta-hydroxybutyrate were normal. Basal cardiac glucose transport and GLUT1 expression were both increased approximately 3-fold in G4H(-/-) mice, but insulin-stimulated glucose uptake was abolished. G4H(-/-) mice develop modest cardiac hypertrophy associated with increased myocyte size and induction of atrial natriuretic and brain natriuretic peptide gene expression in the ventricles. Myocardial fibrosis did not occur. Basal and isoproterenol-stimulated isovolumic contractile performance was preserved. Thus, selective ablation of GLUT4 in the heart initiates a series of events that results in compensated cardiac hypertrophy.
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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.