Evidence map›Paper›PMID 36031603›Full record

ArticleBMC medical genomics2022

Impact of the interaction between the polymorphisms and hypermethylation of the CD36 gene on a new biomarker of type 2 diabetes mellitus: circulating soluble CD36 (sCD36) in Senegalese females.

Maïmouna Touré, Abdoulaye Samb, Mbaye Sène, Souleymane Thiam, Cheikh A B Mané, Abdou K Sow, Awa Ba-Diop, Modou O Kane, Mamadou Sarr, Abdoulaye Ba and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medical genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 38% 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.

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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Impacts ofCardiovascular therapeutics · 2025
    Pooled it
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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

11 authors at 2 institutions in 1 country.

Maïmouna TouréLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal. drmaimounatoure@gmail.com.
Abdoulaye SambLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Mbaye SèneLaboratoire de Physiologie Pharmaceutique, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Souleymane ThiamLaboratoire de Biochimie et de Biologie Moléculaire, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Cheikh A B ManéLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Abdou K SowLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Awa Ba-DiopDepartement de Médecine, Université Alioune Diop de Bambey, Diourbel, Sénégal.
Modou O KaneLaboratoire de Physiologie Pharmaceutique, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Mamadou SarrLaboratoire de Physiologie Pharmaceutique, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Abdoulaye BaLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Lamine GueyeLaboratoire de Physiologie Humaine et d'Explorations Fonctionnelles, Faculté de Médecine, de Pharmacie et d'Odonto-Stomatologie (FMPOS), de l'Université Cheikh Anta Diop (UCAD), Dakar, Sénégal.
Cheikh Anta Diop University · SNUniversité Alioune Diop de Bambey · SN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral predisposing factors for diabetes mellitus have been identified, including cluster determinant 36 (CD36) receptor expression. We aimed to determine the effects of CD36 gene polymorphisms and hypermethylation on the plasma CD36 protein levels in type 2 diabetes. MATERIALS AND

methodsWe conducted a cross-sectional study involving 100 females (lean healthy control subjects and subjects with type 2 diabetes). This study was conducted at the Human Physiology Laboratory at the Dakar Faculty of Medicine in Senegal. Circulating sCD36 levels and DNA methyltransferase 3a levels were determined by enzyme-linked immunosorbent assay. The other biological parameters were evaluated in a biochemical laboratory. CD36 gene polymorphisms and methylation were explored by real-time polymerase chain reaction and methylation-specific polymerase chain reaction, respectively.

resultssCD36 was negatively correlated with HDL-cholesterol levels (r =  - 0.52 p = 0.0001) and triglyceride levels (r =  - 0.36 p = 0.01) in control subjects. However, in the type 2 diabetes group, sCD36 levels were positively correlated with total cholesterol levels (r = 0.28 p = 0.04). For rs3211867, control subjects harboring the CC genotypes had significantly higher sCD36 levels than control subjects harboring the AA/AC genotype (p = 0.02); in the type 2 diabetes group, the sCD36 level was not significantly lower in subjects harboring the AA/AC genotype than in subjects harboring the CC genotype (p = 0.27). CD36 gene methylation reduced the sCD36 level in the control subjects compared to control subjects without CD36 gene methylation (p = 0.03). This difference was not significant in the type 2 diabetes group comparing subjects with diabetes with CD36 gene methylation to subjects with diabetes without CD36 gene methylation (p = 0.09). We noted a nonsignificant increase in sCD36 levels in subjects with diabetes with CD36 gene methylation compared to control subjects with CD36 gene methylation (p = 0.27). A combination of the CD36 polymorphism effect and the CD36 methylation effect did not significantly reduce sCD36 levels in subjects with type 2 diabetes.

conclusionCD36 gene polymorphisms and CD36 gene methylation separately reduce sCD36 levels. Their impacts are compensated for in subjects with type 2 diabetes by an increase in sCD36 levels, the mechanism of which needs to be elucidated.

Indexed as

CD36 AntigensDiabetes Mellitus, Type 2BiomarkersCholesterolCross-Sectional StudiesDNA MethylationFemaleHumansPolymorphism, GeneticSenegalBiomarkersCD36 AntigensCholesterolDNA methylationGenetic polymorphismsCD36 proteinType 2 diabetes

Identifiers

PMID36031603
PMCPMC9422098
OpenAlexW4293523027

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Registered trials

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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.