TNF A −308G&gt;A polymorphism in Moroccan patients with type 2 diabetes mellitus: a case–control study and meta-analysis

Sefri, Hajar; Benrahma, Houda; Charoute, Hicham; yaagoubi, Fouzia Lakbakbi el; Rafiey, Hassan; Lyoussi, Badiâa; Nourlil, Jalal; Abidi, Omar; Barakat, Abdelhamid

doi:10.1007/s11033-014-3454-5

Cited by 9 publications

(4 citation statements)

References 36 publications

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“…Finally, five studies reported data that directly relate polymorphism in question with T2DM (Shiau et al [13], Bouhaha et al [15], Guzmán-Flores et al [16], Saxena et al [19], and Sefri et al [20]), one of which also relates it with obese T2DM patients (Bouhaha et al [15]). The general characteristics of the studies included in this review are summarized in Table 1.…”

Section: Resultsmentioning

confidence: 99%

“…In three studies conducted in Spain, Hungary, and Morocco significant associations between the TNFA -308G/A polymorphism and the risk of T2DM were identified [11, 17, 20]: two of them in patients with other comorbidities such as coronary heart disease [11] and atherosclerosis [17]. …”

Section: Resultsmentioning

confidence: 99%

“…Sefri et al [20] in their meta-analysis, which considers 21 case-control studies published until August 2013, argue that no significant associations were found between the polymorphism in the studied region of the TNFA gene and risk of developing T2DM. Their finding was consistent with a previous meta-analysis, which included data from 18 association studies [46].…”

Section: Discussionmentioning

confidence: 99%

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Association between -308G/A TNFA Polymorphism and Susceptibility to Type 2 Diabetes Mellitus: A Systematic Review

Luna

Silva

Sanchez

2016

Journal of Diabetes Research

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Diabetes mellitus (DM) is considered to be a worldwide epidemic disease and its type 2 form comprises more than 95% of all cases. Tumor necrosis factor-alpha (TNF-α) is a proinflammatory cytokine. Its dysregulation has been implicated in a variety of human diseases, including type 2 diabetes mellitus (T2DM). The control of expression of this cytokine is associated with insulin resistance and has a strong genetic influence. In order to understand this relationship, the literature from all case-control studies since 2000 to date was reviewed. The genotypes frequency results presented in ten publications with different ethnicities were compared. The correlation between the TNFA promoter genotypes and the risk of developing T2DM remains controversial due to the many discrepancies between the different studies available. Ethnic differences may play a role in these conflicting results, since the distribution of TNFA promoter polymorphisms is distinctive between individuals of dissimilar racial origin. Hence, although the relationship between T2DM incidence and presence of polymorphisms at position -308 of the TNFA gene is not entirely clear, the results of these studies suggest the need for further investigation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Association between -308G/A TNFA Polymorphism and Susceptibility to Type 2 Diabetes Mellitus: A Systematic Review

Luna

Silva

Sanchez

2016

Journal of Diabetes Research

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“…The -308 G-->A polymorphism of the TNFA promoter gene is involved in the pathophysiology of insulin resistance and GD [ 41 ]. The same polymorphism is a genetic risk factor for the development of type 2 DM [ 42 ]. Individuals who carry the -308A TNFA gene variant have a 23% greater risk of developing obesity compared with controls, and they showed significantly higher systolic arterial blood pressure and plasma insulin levels, supporting the hypothesis that the TNFA gene is involved in the pathogenesis of the metabolic syndrome [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular association of pathogenetic contributors to pre-eclampsia (pre-eclampsia associome)

et al. 2015

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BackgroundPre-eclampsia is the most common complication occurring during pregnancy. In the majority of cases, it is concurrent with other pathologies in a comorbid manner (frequent co-occurrences in patients), such as diabetes mellitus, gestational diabetes and obesity. Providing bronchial asthma, pulmonary tuberculosis, certain neurodegenerative diseases and cancers as examples, we have shown previously that pairs of inversely comorbid pathologies (rare co-occurrences in patients) are more closely related to each other at the molecular genetic level compared with randomly generated pairs of diseases. Data in the literature concerning the causes of pre-eclampsia are abundant. However, the key mechanisms triggering this disease that are initiated by other pathological processes are thus far unknown. The aim of this work was to analyse the characteristic features of genetic networks that describe interactions between comorbid diseases, using pre-eclampsia as a case in point.ResultsThe use of ANDSystem, Pathway Studio and STRING computer tools based on text-mining and database-mining approaches allowed us to reconstruct associative networks, representing molecular genetic interactions between genes, associated concurrently with comorbid disease pairs, including pre-eclampsia, diabetes mellitus, gestational diabetes and obesity. It was found that these associative networks statistically differed in the number of genes and interactions between them from those built for randomly chosen pairs of diseases. The associative network connecting all four diseases was composed of 16 genes (PLAT, ADIPOQ, ADRB3, LEPR, HP, TGFB1, TNFA, INS, CRP, CSRP1, IGFBP1, MBL2, ACE, ESR1, SHBG, ADA). Such an analysis allowed us to reveal differential gene risk factors for these diseases, and to propose certain, most probable, theoretical mechanisms of pre-eclampsia development in pregnant women. The mechanisms may include the following pathways: [TGFB1 or TNFA]-[IL1B]-[pre-eclampsia]; [TNFA or INS]-[NOS3]-[pre-eclampsia]; [INS]-[HSPA4 or CLU]-[pre-eclampsia]; [ACE]-[MTHFR]-[pre-eclampsia].ConclusionsFor pre-eclampsia, diabetes mellitus, gestational diabetes and obesity, we showed that the size and connectivity of the associative molecular genetic networks, which describe interactions between comorbid diseases, statistically exceeded the size and connectivity of those built for randomly chosen pairs of diseases. Recently, we have shown a similar result for inversely comorbid diseases. This suggests that comorbid and inversely comorbid diseases have common features concerning structural organization of associative molecular genetic networks.

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Genetic variants of tumor necrosis factor-α -308G/A (rs1800629) but not Toll-interacting proteins or vitamin D receptor genes enhances susceptibility and severity of malaria infection

et al. 2017

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Susceptibility to malaria infection has been associated with host genetic polymorphisms that differs between groups. We hypothesize that Toll-interacting proteins (TOLLIP), vitamin D receptor (VDR) and tumor necrosis factor-α (TNF) genes are significant contributors to susceptibility and disease severity in Plasmodium falciparum (Pf) infection. Our aim is to explore the genomic diversity and haplotype frequency of these genes, as well as extrapolate possible association with markers of severity, between malaria-infected and healthy controls. Genomic DNA samples extracted from the blood of 107 malaria-infected patients and 190 uninfected controls were analyzed, with no difference in genotypic or allelic frequencies of TOLLIP and VDR polymorphisms. However, a significant difference in the genotypic (p = 2.20E-16) and allelic frequencies (p = 2.20E-16) of the TNF-α (snp rs1800629) polymorphism was found. The preponderance of the mutant variant among the malaria-infected show a possible impaired capacity to mount an effective immune response, potentially confirmed by our association results. This result calls for analysis of clearly delineated uncomplicated versus severe disease groups, including serum assays, providing a basis to conclude that susceptibility to malaria infection and potential contribution to disease severity is significantly associated with polymorphisms of the tumor necrosis factor-α but not TOLLIP or VDR genes.

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TNF A −308G>A polymorphism in Moroccan patients with type 2 diabetes mellitus: a case–control study and meta-analysis

Cited by 9 publications

References 36 publications

Association between -308G/A TNFA Polymorphism and Susceptibility to Type 2 Diabetes Mellitus: A Systematic Review

Association between -308G/A TNFA Polymorphism and Susceptibility to Type 2 Diabetes Mellitus: A Systematic Review

Molecular association of pathogenetic contributors to pre-eclampsia (pre-eclampsia associome)

Genetic variants of tumor necrosis factor-α -308G/A (rs1800629) but not Toll-interacting proteins or vitamin D receptor genes enhances susceptibility and severity of malaria infection

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