ArticleDiabetologia2010
Requirement for distinct vesicle-associated membrane proteins in insulin- and AMP-activated protein kinase (AMPK)-induced translocation of GLUT4 and CD36 in cultured cardiomyocytes.
Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 121 citations in OpenAlex.
- Integrin-linked kinase promotes hepatic fat accumulation via F-actin stabilization-dependent CD36 plasma membrane localization.iScience · 2026Article
- CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026Review
- Insights into protein synthesis dynamics of gilts from the same genetic background and age differing in protein deposition.Scientific reports · 2026Article
- Integrated analysis of the adipocyte plasma membrane proteome reveals KCC1 and PIT2 as novel insulin-responsive transporters.The Journal of biological chemistry · 2026Article
- Phosphatidylinositol 4-Kinase IIIβ: A Therapeutic Target for Contractile Dysfunction in Hypertrophic Cardiomyocytes.International journal of molecular sciences · 2026Article
- Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025Review
- Alteration of cardiac energetics and mitochondrial function in doxorubicin‑induced cardiotoxicity: Molecular mechanism and prospective implications (Review).International journal of molecular medicine · 2025Review
- Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.Nature communications · 2025Article
- Article
- VAMP5 and distinct sets of cognate Q-SNAREs mediate exosome release.Cell structure and function · 2023Article
- Adiponectin Enhances Fatty Acid Signaling in Human Taste Cells by Increasing Surface Expression of CD36.International journal of molecular sciences · 2023Article
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021Article
- CD36 Signal Transduction in Metabolic Diseases: Novel Insights and Therapeutic Targeting.Cells · 2021Review
- Insulin signaling in the heart.American journal of physiology. Endocrinology and metabolism · 2021Review
- CD36 Signaling in Diabetic Cardiomyopathy.Aging and disease · 2021Review
- Distinct signaling by insulin and IGF-1 receptors and their extra- and intracellular domains.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Metabolic Interventions to Prevent Hypertrophy-Induced Alterations in Contractile Properties In Vitro.International journal of molecular sciences · 2021Article
- Phosphatidylinositol 4-kinase IIIβ mediates contraction-induced GLUT4 translocation and shows its anti-diabetic action in cardiomyocytes.Cellular and molecular life sciences : CMLS · 2021Article
- New insight in understanding the contribution of SGLT1 in cardiac glucose uptake: evidence for a truncated form in mice and humans.American journal of physiology. Heart and circulatory physiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisUpon stimulation of insulin signalling or contraction-induced AMP-activated protein kinase (AMPK) activation, the glucose transporter GLUT4 and the long-chain fatty acid (LCFA) transporter CD36 similarly translocate from intracellular compartments to the plasma membrane of cardiomyocytes to increase uptake of glucose and LCFA, respectively. This similarity in regulation of GLUT4 traffic and CD36 traffic suggests that the same families of trafficking proteins, including vesicle-associated membrane proteins (VAMPs), are involved in both processes. While several VAMPs have been implicated in GLUT4 traffic, nothing is known about the putative function of VAMPs in CD36 traffic. Therefore, we compared the involvement of the myocardially produced VAMP isoforms in insulin- or contraction-induced GLUT4 and CD36 translocation.
methodsFive VAMP isoforms were silenced in HL-1 cardiomyocytes. The cells were treated with insulin or the contraction-like AMPK activator oligomycin or were electrically stimulated to contract. Subsequently, GLUT4 and CD36 translocation as well as substrate uptake were measured.
resultsThree VAMPs were demonstrated to be necessary for both GLUT4 and CD36 translocation, either specifically in insulin-treated cells (VAMP2, VAMP5) or in oligomycin/contraction-treated cells (VAMP3). In addition, there are VAMPs specifically involved in either GLUT4 traffic (VAMP7 mediates basal GLUT4 retention) or CD36 traffic (VAMP4 mediates insulin- and oligomycin/contraction-induced CD36 translocation). CONCLUSIONS/
interpretationThe involvement of distinct VAMP isoforms in both GLUT4 and CD36 translocation indicates that CD36 translocation, just like GLUT4 translocation, is a vesicle-mediated process dependent on soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex formation. The ability of other VAMPs to discriminate between GLUT4 and CD36 translocation allows the notion that myocardial substrate preference can be modulated by these VAMPs.
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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.