Evidence map›Paper›PMID 20333349›Full record

ArticleDiabetologia2010

Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients.

C Aguer, J Mercier, C Yong Wai Man, L Metz, S Bordenave, K Lambert, E Jean, L Lantier, L Bounoua, J F Brun and 4 more

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Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
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48citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed.

  1. Trial
  2. Enhanced ECCD36 signaling promotes skeletal muscle insulin resistance in female mice.American journal of physiology. Endocrinology and metabolism · 2024
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  3. Review
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  11. Effects of PCB126 on Adipose-to-Muscle Communication in anEnvironmental health perspectives · 2020
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Polychlorinated biphenyl 126 exposure in rats alters skeletal muscle mitochondrial function.Environmental science and pollution research international · 2019
    Article
  18. Review
  19. Article
  20. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

C AguerINSERM, ERI25 Muscle et pathologies, Hôpital A. de Villeneuve, Bâtiment Crastes de Paulet, Avenue du Doyen G. Giraud, Montpellier F-34295, France.
J Mercier
C Yong Wai Man
L Metz
S Bordenave
K Lambert
E Jean
L Lantier
L Bounoua
J F Brun
E Raynaud de Mauverger
F Andreelli
M Foretz
M Kitzmann

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisIntramyocellular lipids (IMCL) accumulation is a classical feature of metabolic diseases. We hypothesised that IMCL accumulate mainly as a consequence of increased adiposity and independently of type 2 diabetes. To test this, we examined IMCL accumulation in two different models and four different populations of participants: muscle biopsies and primary human muscle cells derived from non-obese and obese participants with or without type 2 diabetes. The mechanism regulating IMCL accumulation was also studied.

methodsMuscle biopsies were obtained from ten non-obese and seven obese participants without type 2 diabetes, and from eight non-obese and eight obese type 2 diabetic patients. Mitochondrial respiration, citrate synthase activity and both AMP-activated protein kinase and acetyl-CoA carboxylase phosphorylation were measured in muscle tissue. Lipid accumulation in muscle and primary myotubes was estimated by Oil Red O staining and fatty acid translocase (FAT)/CD36 localisation by immunofluorescence.

resultsObesity and type 2 diabetes are independently characterised by skeletal muscle IMCL accumulation and permanent FAT/CD36 relocation. Mitochondrial function is not reduced in type 2 diabetes. IMCL accumulation was independent of type 2 diabetes in cultured myotubes and was correlated with obesity markers of the donor. In obese participants, membrane relocation of FAT/CD36 is a determinant of IMCL accumulation. CONCLUSIONS/

interpretationIn skeletal muscle, mitochondrial function is normal in type 2 diabetes, while IMCL accumulation is dependent upon obesity or type 2 diabetes and is related to sarcolemmal FAT/CD36 relocation. In cultured myotubes, IMCL content and FAT/CD36 relocation are independent of type 2 diabetes, suggesting that distinct factors in obesity and type 2 diabetes contribute to permanent FAT/CD36 relocation ex vivo.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnalysis of VarianceBlotting, WesternBody Fat DistributionCD36 AntigensCells, CulturedCitrate (si)-SynthaseDiabetes Mellitus, Type 2Fluorescent Antibody TechniqueHumansLipidsMaleMiddle AgedMitochondriaMuscle, SkeletalAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesCD36 AntigensCitrate (si)-SynthaseLipids

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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.