ArticleThe Journal of biological chemistry2012
Overexpression of vesicle-associated membrane protein (VAMP) 3, but not VAMP2, protects glucose transporter (GLUT) 4 protein translocation in an in vitro model of cardiac insulin resistance.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 56 citations in OpenAlex.
- The Umbelliprenin-CTAB cellulose nanocrystal delivery system prevents hyperglycemia in diabetic rats by activating the insulin receptor IR/PDK1 pathway.Scientific reports · 2025Article
- Induction on Insulin Resistance In Vitro.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- miR-124 and VAMP3 Act Antagonistically in Human Neuroblastoma.International journal of molecular sciences · 2023Article
- Modelling Diabetic Cardiomyopathy: Using Human Stem Cell-Derived Cardiomyocytes to Complement Animal Models.Metabolites · 2022Review
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- Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021Article
- Insulin signaling in the heart.American journal of physiology. Endocrinology and metabolism · 2021Review
- Considerations for using isolated cell systems to understand cardiac metabolism and biology.Journal of molecular and cellular cardiology · 2021Review
- Metformin downregulates miR223 expression in insulin-resistant 3T3L1 cells and human diabetic adipose tissue.Endocrine · 2020Article
- Hepatocyte TMEM16A Deletion Retards NAFLD Progression by Ameliorating Hepatic Glucose Metabolic Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Exogenous HAging and disease · 2020Article
- Augmenting Vacuolar HInternational journal of molecular sciences · 2020Article
- Cardiac SNARE Expression in Health and Disease.Frontiers in endocrinology · 2019Article
- Fatty Acids Prevent Hypoxia-Inducible Factor-1α Signaling Through Decreased Succinate in Diabetes.JACC. Basic to translational science · 2018Article
- Sitagliptin improved glucose assimilation in detriment of fatty-acid utilization in experimental type-II diabetes: role of GLP-1 isoforms in Glut4 receptor trafficking.Cardiovascular diabetology · 2018Article
- The Popeye Domain Containing Genes and their Function in Striated Muscle.Journal of cardiovascular development and disease · 2016Article
- Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association.Circulation research · 2016Review
- Article
- A Lead ANRIL Polymorphism Is Associated with Elevated CRP Levels in Periodontitis: A Pilot Case-Control Study.PloS one · 2015Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac glucose utilization is regulated by reversible translocation of the glucose transporter GLUT4 from intracellular stores to the plasma membrane. During the onset of diet-induced insulin resistance, elevated lipid levels in the circulation interfere with insulin-stimulated GLUT4 translocation, leading to impaired glucose utilization. Recently, we identified vesicle-associated membrane protein (VAMP) 2 and 3 to be required for insulin- and contraction-stimulated GLUT4 translocation, respectively, in cardiomyocytes. Here, we investigated whether overexpression of VAMP2 and/or VAMP3 could protect insulin-stimulated GLUT4 translocation under conditions of insulin resistance. HL-1 atrial cardiomyocytes transiently overexpressing either VAMP2 or VAMP3 were cultured for 16 h with elevated concentrations of palmitate and insulin. Upon subsequent acute stimulation with insulin, we measured GLUT4 translocation, plasmalemmal presence of the fatty acid transporter CD36, and myocellular lipid accumulation. Overexpression of VAMP3, but not VAMP2, completely prevented lipid-induced inhibition of insulin-stimulated GLUT4 translocation. Furthermore, the plasmalemmal presence of CD36 and intracellular lipid levels remained normal in cells overexpressing VAMP3. However, insulin signaling was not retained, indicating an effect of VAMP3 overexpression downstream of PKB/Akt. Furthermore, we revealed that endogenous VAMP3 is bound by the contraction-activated protein kinase D (PKD), and contraction and VAMP3 overexpression protect insulin-stimulated GLUT4 translocation via a common mechanism. These observations indicate that PKD activates GLUT4 translocation via a VAMP3-dependent trafficking step, which pathway might be valuable to rescue constrained glucose utilization in the insulin-resistant heart.
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