ArticlePloS one2011
Increased FAT/CD36 cycling and lipid accumulation in myotubes derived from obese type 2 diabetic patients.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05671614 (Skeletal Muscle Regeneration in Survivors of Critical Illness), which is not on this map. Cited by 20 papers.
What it found
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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.
Skeletal Muscle Regeneration in Survivors of Critical Illness: How to Prevent Satellite Cell Failure?
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- CD36 and Its Role in Obesity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Targeting Inflammation with Dietary ω-3 Polyunsaturated Fatty Acids Improved Lipid Mobilization and Flux in Heat-Stressed Wether Lambs.Metabolites · 2026Article
- Myokine Secretion following an Aerobic Exercise Intervention in Individuals with Type 2 Diabetes with or without Exercise Resistance.International journal of molecular sciences · 2024Article
- RabGAP AS160/TBC1D4 deficiency increases long-chain fatty acid transport but has little additional effect on obesity and metabolic syndrome in ADMSCs-derived adipocytes of morbidly obese women.Frontiers in molecular biosciences · 2023Article
- Grape Polyphenols in the Treatment of Human Skeletal Muscle Damage Due to Inflammation and Oxidative Stress during Obesity and Aging: Early Outcomes and Promises.Molecules (Basel, Switzerland) · 2022Review
- The mesoionic compound MI-D changes energy metabolism and induces apoptosis in T98G glioma cells.Molecular and cellular biochemistry · 2022Article
- Diabetic Conditions Confer Metabolic and Structural Modifications to Tissue-Engineered Skeletal Muscle.Tissue engineering. Part A · 2021Article
- Review
- Article
- Lipid oversupply induces CD36 sarcolemmal translocation via dual modulation of PKCζ and TBC1D1: an early event prior to insulin resistance.Theranostics · 2020Article
- Dynamic role of the transmembrane glycoprotein CD36 (SR-B2) in cellular fatty acid uptake and utilization.Journal of lipid research · 2018Review
- The Effect of Hypoxia and Metformin on Fatty Acid Uptake, Storage, and Oxidation in L6 Differentiated Myotubes.Frontiers in endocrinology · 2018Article
- The Implication of PGC-1α on Fatty Acid Transport across Plasma and Mitochondrial Membranes in the Insulin Sensitive Tissues.Frontiers in physiology · 2017Review
- Ca2+ Binding/Permeation via Calcium Channel, CaV1.1, Regulates the Intracellular Distribution of the Fatty Acid Transport Protein, CD36, and Fatty Acid Metabolism.The Journal of biological chemistry · 2015Article
- Factors influencing the eicosanoids synthesis in vivo.BioMed research international · 2015Review
- c-Myc programs fatty acid metabolism and dictates acetyl-CoA abundance and fate.The Journal of biological chemistry · 2014Article
- Adipose and muscle tissue profile of CD36 transcripts in obese subjects highlights the role of CD36 in fatty acid homeostasis and insulin resistance.Diabetes care · 2014Article
- Reduced incorporation of fatty acids into triacylglycerol in myotubes from obese individuals with type 2 diabetes.Diabetes · 2014Article
- Lipid in skeletal muscle myotubes is associated to the donors' insulin sensitivity and physical activity phenotypes.Obesity (Silver Spring, Md.) · 2014Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPermanent fatty acid translocase (FAT/)CD36 relocation has previously been shown to be related to abnormal lipid accumulation in the skeletal muscle of type 2 diabetic patients, however mechanisms responsible for the regulation of FAT/CD36 expression and localization are not well characterized in human skeletal muscle. METHODOLOGY/PRINCIPAL
findingsPrimary muscle cells derived from obese type 2 diabetic patients (OBT2D) and from healthy subjects (Control) were used to examine the regulation of FAT/CD36. We showed that compared to Control myotubes, FAT/CD36 was continuously cycling between intracellular compartments and the cell surface in OBT2D myotubes, independently of lipid raft association, leading to increased cell surface FAT/CD36 localization and lipid accumulation. Moreover, we showed that FAT/CD36 cycling and lipid accumulation were specific to myotubes and were not observed in reserve cells. However, in Control myotubes, the induction of FAT/CD36 membrane translocation by the activation of (AMP)-activated protein kinase (AMPK) pathway did not increase lipid accumulation. This result can be explained by the fact that pharmacological activation of AMPK leads to increased mitochondrial beta-oxidation in Control cells. CONCLUSION/SIGNIFICANCE: Lipid accumulation in myotubes derived from obese type 2 diabetic patients arises from abnormal FAT/CD36 cycling while lipid accumulation in Control cells results from an equilibrium between lipid uptake and oxidation. As such, inhibiting FAT/CD36 cycling in the skeletal muscle of obese type 2 diabetic patients should be sufficient to diminish lipid accumulation.
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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.