Evidence map›Paper›PMID 28729885›Full record

ArticleDiabetology & metabolic syndrome2017

CD36 overexpression: a possible etiopathogenic mechanism of atherosclerosis in patients with prediabetes and diabetes.

M D Lopez-Carmona, M C Plaza-Seron, A Vargas-Candela, F J Tinahones, R Gomez-Huelgas, M R Bernal-Lopez

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06881706 (Relationship Between Biochemical and Anthropometric Variables and CD36 Levels in Metabolic Syndrome Patients After Low Calorie Diet), which is not on this map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

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

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.

NCT06881706 nacompletednot on this mapstarted 2019, after this paper: background citation

Relationship Between Biochemical and Anthropometric Variables and CD36 Levels in Metabolic Syndrome Patients After Low Calorie Diet

TypeinterventionalSponsorOrdu UniversityRan2019 to 2020Enrolled65ConditionsMetabolic Syndrome, Weight LossArmsmedical nutrition therapy
3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Observational
  5. The Mechanisms of the Development of Atherosclerosis in Prediabetes.International journal of molecular sciences · 2021
    Review
  6. Role of the Scavenger Receptor CD36 in Accelerated Diabetic Atherosclerosis.International journal of molecular sciences · 2020
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

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

6 authors at 2 institutions in 1 country.

M D Lopez-CarmonaInternal Medicine Department, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Carlos Haya Hospital), Avda. Hospital Civil s/n, 29009 Malaga, Spain.
M C Plaza-SeronResearch Laboratory-Allergy Unit, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Carlos Haya Hospital), Malaga, Spain.
A Vargas-CandelaInternal Medicine Department, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Carlos Haya Hospital), Avda. Hospital Civil s/n, 29009 Malaga, Spain.
F J TinahonesEndocrinology and Nutrition Department, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Virgen de la Victoria Hospital), Malaga, Spain.
R Gomez-HuelgasInternal Medicine Department, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Carlos Haya Hospital), Avda. Hospital Civil s/n, 29009 Malaga, Spain.
M R Bernal-LopezInternal Medicine Department, Biomedical Institute of Malaga (IBIMA), Regional University Hospital of Malaga (Carlos Haya Hospital), Avda. Hospital Civil s/n, 29009 Malaga, Spain.
Instituto de Investigación Biomédica de Málaga · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleCD36 is a scavenger receptor located on monocytes which is involved in foam cell transformation.

aimTo evaluate CD36 expression under different glycemic states in both healthy subjects and in atherosclerotic patients. SUBJECTS AND

methodsIn order to evaluate the possible effects of hyperglycemia on CD36 expression in healthy subjects, an in vitro experiment was carried out using monocyte in three different conditions: extreme hyperglycemia (HG), euglycemia (EG) and in the absence of glucose. On the other hand, three groups of atherosclerotic patients were evaluated according to their glycemic conditions: normoglycemic (NG), prediabetic (preDM) and diabetic (DM) patients. CD36 expression (mRNA, non-glycated and glycated protein) was analyzed in monocytes.

resultsCD36 mRNA expression in the in vitro experiment peaked at 4 and 24 h under HG conditions. No differences in mRNA levels were found in the EG and control group. The level of non-glycated proteins was higher in HG and EG conditions compared with control group. Glycated protein expression was inhibited by glucose in a sustained manner. In atherosclerotic patients, a significant association was observed when comparing glycated CD36 protein expression in DM with NG patients (p = 0.03). No significant differences were found in mRNA and non-glycated CD36 expression in these patients. Moreover, BMI, insulin, weight and treatment were shown to be related to CD36 expression (mRNA, non-glycated and glycated protein levels, depending of the case) in atherosclerotic patients.

conclusionsHyperglycemia is an important modulator of CD36 mRNA and non-glycated protein expression in vitro, increasing de novo synthesis in healthy subjects. In atherosclerotic patients, there are progressive increases in CD36 receptors, which may be due to a post-translational stimulus.

Indexed as

AtherosclerosisCD36 receptorHuman clinicalMonocytesType 2 diabetes

Identifiers

PMID28729885
PMCPMC5516302
OpenAlexW2739100321

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.