Evidence map›Paper›PMID 38243005›Full record

ArticleBiochemical genetics2024

Genetic Investigation of the Trail Mechanism in Diabetic and Non-diabetic Obese Patients.

Saadet Busra Aksoyer Sezgin, Sermin Durak, Faruk Celik, Arezoo Gheybi, Murat Diramali, Ramazan Cakmak, Ali Osman Gurol, Ilhan Yaylim, Umit Zeybek

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In one paragraph

Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

9 authors at 5 institutions in 2 countries.

Saadet Busra Aksoyer SezginDepartment of Medical Biology and Genetics, Faculty of Medicine, Istanbul Yeni Yuzyil University, 34010, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-8338-9546
Sermin DurakDepartment of Medical Microbiology, Faculty of Medicine, Istanbul University Cerrahpasa, 34098, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-6741-4345
Faruk CelikDepartment of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, 34093, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-2433-0277
Arezoo GheybiDepartment of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, 34093, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-6167-7571
Murat DiramaliDepartment of Anatomy, Faculty of Medicine, Bolu Abant Izzet Baysal University, 14030, Bolu, Turkey.ORCID http://orcid.org/0000-0001-5824-6159
Ramazan CakmakDepartment of Internal Decease, Istanbul University, 34093, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-3815-7444
Ali Osman GurolDepartment of Immunology, Aziz Sancar Institute of Experimental Medicine, Istanbul University, 34093, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-6682-4289
Ilhan YaylimDepartment of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, 34093, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-2615-0202
Umit ZeybekDepartment of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, 34093, Istanbul, Turkey. umz67@yahoo.com.ORCID http://orcid.org/0000-0001-8403-2939
Istanbul University · TRBolu Abant İzzet Baysal University · TRHUN-REN Institute of Experimental Medicine · HUIstanbul University-Cerrahpaşa · TRIstanbul Yeni Yüzyıl University · TR

Funding

Istanbul University Scientific Research Projects Unit Project Number: TDK-2020-36578
6 · The paper itself

Abstract

Obesity is an important healthcare issue caused by abnormally increased adipose tissue because of energy-intake overcoming energy expenditure. Disturbances in the physiological function of adipose tissue mediate the development of diabetes. It is a metabolic disease that results from decreased insulin-levels and/or changes in the insulin action mechanism. Tumor Necrosis Factor-Associated Apoptosis-Inducing Ligand(TRAIL), which is a member of the Tumor Necrosis Factor(TNF)-family with an important role in adipose tissue biology, is included in many studies with its ability to induce apoptosis in cancer cells, but the number of human-studies conducted on the gene related to its protective-role against diabetes and obesity at this level is insufficient. Our study was carried out as a case and control and included three groups (80 diabetic obese, 80 non-diabetic obese, and 80 healthy individuals as the control group). The Real-Time-PZR(RT-qPZR), and DNA Sanger-Sequencing Methods were used for gene expression and gene squences. As a result of the analyses, TRAIL gene expression level was found to be higher in the controls than in the diabetic-obese and non-diabetic-obese group. This change in TRAIL gene expression suggests that TRAIL maybe a protective factor against diabetes. The presence of rs781673405, rs143353036, rs1244378045, rs767450259, rs759369504, rs750556128, and rs369143448 mutations, which was determined with the Sequencing-Method, was shown for the first time in the present study. In addition, it is the first study in which human TRAIL gene-expression and sequencing were performed together. We believe that these data will make an important contribution to the literature.

Indexed as

ObesityTNF-Related Apoptosis-Inducing LigandAdultCase-Control StudiesDiabetes MellitusDiabetes Mellitus, Type 2FemaleHumansMaleMiddle AgedPolymorphism, Single NucleotideTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanDiabetesExpressionObesitySanger sequencingTRAIL

Identifiers

PMID38243005
OpenAlexW4391017444

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.