ArticlePflugers Archiv : European journal of physiology2019
Chronic AICAR treatment prevents metabolic changes in cardiomyocytes exposed to free fatty acids.
Article in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- AICAr, a Widely Used AMPK Activator with Important AMPK-Independent Effects: A Systematic Review.Cells · 2021Pooled it
- AMPK Signalling in Heart Failure: From Metabolic Sensor to Context-Dependent Therapeutic Target.Biomedicines · 2026Review
- NADMetabolites · 2025Article
- Delayed metabolic disturbances in the myocardium after exertional heat stroke: contrasting effects of exertion and thermal load.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Free fatty acids induce coronary microvascular dysfunction via inhibition of the AMPK/KLF2/eNOS signaling pathway.International journal of molecular medicine · 2023Article
- AICAR Improves Outcomes of Metabolic Syndrome and Type 2 Diabetes Induced by High-Fat Diet in C57Bl/6 Male Mice.International journal of molecular sciences · 2022Article
- Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress.International journal of molecular sciences · 2021Review
- Relationships between constituents of energy drinks and beating parameters in human induced pluripotent stem cell (iPSC)-Derived cardiomyocytes.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Mitochondrial ROS Formation in the Pathogenesis of Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2020Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The stimulation of glucose transport by metabolic stress is an important determinant of myocardial susceptibility to ischemia and reperfusion injury. Stimulation of glucose transport is markedly impaired in cardiomyocytes chronically exposed to excess free fatty acids (FFA), as occurs in vivo in type 2 diabetes. To determine whether chronic low-grade activation of AMP-activated kinase (AMPK) improves substrate metabolism in cardiomyocytes exposed to FFA, isolated cultured cardiomyocytes were exposed for 7 days to FFA ± the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). Glucose transport and glycolysis were then measured during acute metabolic stress provoked by oligomycin. Chronic treatment with AICAR improved basal and oligomycin-stimulated glucose transport in FFA-exposed but not in control cardiomyocytes. Similarly, basal and oligomycin-stimulated glycolysis was reduced in FFA-exposed cardiomyocytes but restored by chronic AICAR treatment. Conversely, fatty acid oxidation was increased in FFA-exposed cardiomyocytes and reduced by chronic AICAR treatment. Chronic AICAR treatment induced in FFA-exposed cardiomyocytes the biogenesis of numerous lipid droplets. Curiously, whereas acute treatment of cardiomyocytes with AICAR increased phosphorylation of the AMPKα subunit on T
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