scholarly journals Urotensin-II gene rs228648 polymorphism associated with the risk of diabetes mellitus

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Yawei Zhao ◽  
Shuhua Fang ◽  
Kerong Que ◽  
Guangli Xu ◽  
Heng Zhang ◽  
...  

Background: Urotensin-II (UII) rs228648 polymorphism has been reported to be associated with the risk of diabetes mellitus (DM) with inconsistent results. The present study sought to reassess the relationship between this polymorphism and susceptibility to DM by meta-analysis. Methods: Relevant eligible studies and whole genome association study (GWAS) data electronically searched were pooled to evaluate the strength of the association with odds ratios (ORs) and 95% confidence intervals (CIs). Results: Seven case–control studies involving 894 cases and 1186 controls were finally included in the meta-analysis. Overall analyses indicated that UII gene rs228648 variant was significantly associated with reduced risk of DM (allele, A vs. G: OR = 0.68, 95%CI = 0.56–0.82; dominant, AA+GA vs. GG: OR = 0.70, 95%CI = 0.53–0.91; homozygote, AA vs. GG: OR = 0.41, 95%CI = 0.28–0.61; recessive, AA vs. GA+GG: OR = 0.36, 95%CI = 0.19–0.71). In subgroup analyses based on ethnicity, the results showed a significant association of rs228648 polymorphism with decreased risk of DM in Chinese population under all five genetic models as well as in non-Chinese population under heterozygote and recessive models. Stratified analyses by specific type of DM also presented a significant association for common diabetes mellitus (CDM) under allele and homozygote as well as gestational diabetes mellitus (GDM) under all genetic models except for homozygote model. However, the synthetic analysis with GWAS data suggested an increased risk of DM with rs228648 effect allele in European population (OR = 1.01, 95%CI = 1.00–1.02). Conclusion: The present meta-analysis preliminarily suggested a potentially opposite role of rs228648 polymorphism associated with DM risk in the Chinese and European population. Further studies are in great request to verify the results.

2021 ◽  
Author(s):  
Ravi BHUSHAN ◽  
Sonal Upadhyay ◽  
Shally AWASTHI ◽  
Monika Panday

Abstract Background Several molecular epidemiological studies have analyzed the associations between genetic variants and the risk of gestational diabetes mellitus (GDM). However, all these studies suffer from inconsistent and conflicting results owing to relatively smaller sample sizes, fewer genetic variants included in the research, and limited statistical power. Hence, a coherent review and meta-analysis were carried out to provide a quantitative summary related to the associations of commonly studied SNPs with GDM risk. Methods Eligible studies were retrieved from PubMed,updated on Dec. 2019. Based on several inclusion and exclusion criteria, 71 articles with 42928 GDM patients and 77793 controls were finally considered for meta-analysis. The genotype data from 23 variants of sixteen genes were statistically analyzed using RevMan v 5.2 software. Newcastle-Ottawa Scale (NOS) was used to assess the quality of the research article. Heterogeneity among studies was tested by I2 and odds ratio with 95% confidence interval (CI) was carried out for all five genetic models. Results The overall combined odds ratio reveals that variants like MTNR1B (rs1083963, rs1387153), GCK (rs1799884), CANP10 (rs3792267), and GCKR (rs780094) are significantly associated with GDM in all genetic models while CANP10 (rs5030952), ADRB (rs4994) and FTO (rs8050136) are not significantly associated with GDM in any genetic models. Variants MTNR1B (rs1083963, rs1387153) and GCK (rs1799884) are associated with increased risk (OR>1, p<0.05) of GDM, and all these are related to insulin secretion. Other variants related to insulin secretion like TCF7L2 (rs7903146) and SLC30A8 (rs1326634) are also associated with increased risk (OR>1, p<0.05) of GDM. On the contrary, CANP10 (rs3792267) and GCKR (rs780094) are found associated with decreased risk (OR<1, p<0.05) of GDM. Other variants are significantly associated with the GDM in at least one or more genetic models. Conclusion Our study identified that most of the variants related to insulin secretions like MTNR1B (rs1083963), GCK (rs1799884), TCF7L2 (rs7903146), GCKR (rs780094), and SLC30A8 (rs1326634) are more strongly associated (p<0.005) with GDM as compared to the variants related to the insulin resistance like PPARG (rs1801282), IRS1 (rs1801278) and ADIPOQ (rs266729).


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e24101-e24101
Author(s):  
Igal Kushnir ◽  
Dominika Bhatia ◽  
Amirrtha Srikanthan ◽  
Iliana Lega

e24101 Background: Diabetes mellitus (DM) has emerged as a possible late sequela after successfully treating pediatric and young adult (YA) malignancies. We conducted a systematic review and meta-analysis in order to quantify this risk and assess possible risk factors. Methods: We searched MEDLINE and EMBASE databases from inception to April 2019. We included cohort or case-control studies that reported the risk of DM (hazard ratio [HR], relative risk, or odds ratio, and 95% confidence interval [CI]) among childhood and YA cancer survivors ( < age 21 years) compared to those without a history of childhood or YA cancer. We used the Newcastle-Ottawa Score (NOS) to assess risk of bias and study quality. Study effect estimates were pooled using random-effects meta-analyses. Heterogeneity was assessed using the I2 statistic. Results: After applying our exclusion/inclusion criteria, we included 6 articles in our meta-analysis, with a median follow-up time of 11 (range 10-23) years. The median NOS score was 8 (range 7 – 8), indicating high study quality. The risk of DM was significantly higher in childhood and YA cancer survivors relative to controls (HR 1.66, 95% CI 1.54 to 1.79, I2 = 1%). Among cancer types, the highest risk for DM was reported after treatment for leukemia (HR 2.91, 95% CI 2.01 to 4.22 I2 = 75%), lymphoma (HR 1.63, 95% CI 1.37 to 1.94, I2 = 0%) and central nervous system malignancies (HR 1.77, 95% CI 1.30 to 2.39, I2 = 49%), relative to controls. Receiving total body irradiation or abdominal radiation was associated with a DM risk of 4.52 (95% CI 2.29 to 8.93, I2 = 87%), relative to controls. Conclusions: Our meta-analysis demonstrated an increased risk of developing DM among childhood and YA cancer survivors. More emphasis on screening for DM and prevention among this population should be offered.


2016 ◽  
Vol 41 (3-4) ◽  
pp. 119-138 ◽  
Author(s):  
Chunli Chen ◽  
Zhiping Hu

Background and Purpose: Numerous studies have evaluated the association between apolipoprotein E (ApoE) gene polymorphisms and the risk of different subtypes of stroke. However, the results remain uncertain, and few sources of data specific to the Chinese ethnic population contribute to these outstanding questions. Therefore, we performed a meta-analysis to derive a more comprehensive estimate of the association between ApoE polymorphisms and stroke risk in the Chinese population. Methods: Case-control studies in Chinese and English publications were identified by searching the PubMed, EMBASE, Web of Science, China Nation Knowledge Infrastructure Platform, Wanfang, and VIP databases and by hand-searching relevant journals and the reference lists of the retrieved articles. ORs and 95% CIs were applied to assess the strength of the associations. Subgroup and sensitivity analyses were performed to explore between-study heterogeneity. Results: Evidence of a significant association was found between the ApoE ε4 allele and different subtypes of stroke (for ischemic stroke (IS): OR 2.19, 95% CI 1.90-2.52, p < 0.001; for intracerebral hemorrhage (ICH): OR 2.08, 95% CI 1.57-2.75, p < 0.001; and for subarachnoid hemorrhage (SAH): OR 2.03, 95% CI 1.28-3.23, p = 0.003) among the Chinese population. In addition, a significant difference in the risk for different subtypes of stroke between ε4 carriers and ε3ε3 genotype carriers was found (for IS: OR 2.41, 95% CI 2.00-2.89, p < 0.001; for ICH: OR 2.41, 95% CI 1.68-3.47, p < 0.001; and for SAH: OR 2.04, 95% CI 1.21-3.45, p = 0.008). Conclusion: The ApoE ε4 allele may predict an increased risk for different subtypes of stroke, including IS, ICH and SAH, in the Chinese population, and the results of this genotypic analysis may help to identify populations at an increased risk for stroke. Further studies with larger sample sizes are needed to confirm our findings.


2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Li Sun ◽  
Quan Yuan ◽  
Ning Cao ◽  
Wei Guo ◽  
Li Yao ◽  
...  

Objective. This meta-analysis aimed to investigate a comprehensive and reliable conclusion on the correlations of single nucleotide polymorphisms (SNPs) in the vascular endothelial growth factor (VEGF) gene with the risk of diabetic nephropathy (DN) in patients with diabetes mellitus (DM). Methods. We screened PubMed, Embase, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, CBM, and CNKI databases for those relevant studies that investigated the association of 14,945 subjects with clinicopathological parameters in gastric cancer. Results. Eleven case-control studies that met all inclusion criteria were included in this meta-analysis. A total of 14,945 subjects were involved, including 3,049 DN patients and 11,896 DM patients. Our meta-analysis results revealed that VEGF rs2010963 and rs3025039 polymorphisms might contribute to the risk of DN in DM patients. Ethnicity-stratified analysis suggested that VEGF genetic polymorphisms were associated with an increased risk of DN among Asians. However, we found no correlations of VEGF genetic polymorphisms with susceptibility to DN among Caucasians. Conclusion. Our findings suggest that VEGF rs2010963 and rs3025039 polymorphisms may contribute to the risk of DN in DM patients, especially among Asians. Thus, VEGF genetic polymorphisms could be useful biomarkers for early diagnosis of DN in DM patients.


2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Yaqin Tu ◽  
Guorun Fan ◽  
Tianshu Zeng ◽  
Xiong Cai ◽  
Wen Kong

Graves’ disease (GD) is a common autoimmune disorder with a genetic predisposition. Owing to the biological effect of tumor necrosis factor-α (TNF-α) on the thyroid gland and its gene location, TNF-α should be able to influence an individual’s susceptibility to GD. In the present study, we conduct a meta-analysis of rs1800629 and rs361525 in TNF-α gene from all eligible case–control studies to assess the associations amongst reported TNF-α gene with GD. A total of ten case–control studies involving 2790 GD patients and 3472 healthy controls were included. The results showed that a significant association was characterized between the rs1800629 polymorphism and GD in the homozygous model (AA compared with GG: odds ratio (OR) = 1.97, 95% confidence interval (CI) = 1.27–3.06, P=0.002) and recessive model (AA compared with GA + GG: OR = 1.62, 95% CI = 1.04–2.50, P=0.03). GD susceptibility was significantly detected in European population in all genetic models after ethnicity stratification. In sharp contrast, no significant association could be detected in Asian population. Next, we conducted a meta-analysis for another promoter SNP rs361525. However, SNP rs361525 did not show a significant association with GD in any genetic model before and after ethnicity stratification. Together, our data support that only the promoter single-nucleotide polymorphism (SNP) rs1800629 within the TNF-α gene is associated with increased risk for developing GD, especially in European population. Future large-scale studies are required to validate the associations between TNF-α gene and GD.


Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 298 ◽  
Author(s):  
Taheri ◽  
Sarani ◽  
Moazeni-Roodi ◽  
Naderi ◽  
Hashemi

Background and Objectives: Several studies inspected the impact of P2X7 polymorphisms on individual susceptibility to tuberculosis (TB), but the findings are still controversial and inconclusive. To achieve a more precise estimation, we conducted a meta-analysis of all eligible studies on the association between P2X7 polymorphisms and TB risk. Materials and Methods: Relevant studies were identified by searching the PubMed, Web of Science, Scopus and Google scholar databases up to November 2018. Twenty-four full-text articles were included in our meta-analysis. The strength of association between P2X7 polymorphisms and TB risk was evaluated by odds ratios (ORs) and 95% confidence intervals (95% CIs) under five genetic models. Results: The findings of this meta-analysis revealed that the rs3751143 variant significantly increased the risk of TB in heterozygous codominant (OR = 1.44, 95%CI = 1.17−1.78, p = 0.0006, AC vs. AA), homozygous codominant (OR = 1.87, 95% CI = 1.40−2.49, p = 0.0004, CC vs. AA), dominant (OR = 1.50, 95% CI = 1.22−1.85, p = 0.0002, AC + CC vs. AA), recessive (OR = 1.61, 95% CI = 1.25−2.07, p = 0.001, CC vs. AC + AA), and allele (OR = 1.41, 95% CI = 1.19−1.67, p < 0.0001, C vs. A) genetic models. Stratified analysis showed that rs3751143 increased the risk of pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB) in all genetic models. Furthermore, the rs3751143 increased risk of TB in the Asian population. The findings did not support an association between the rs2393799, rs1718119, rs208294, rs7958311, and rs2230911 polymorphisms of P2X7 and TB risk. Conclusions: The findings of this meta-analysis suggest that P2X7 rs3751143 polymorphism may play a role in susceptibility to TB in the Asian population. More well-designed studies are required to elucidate the exact role of P2X7 polymorphisms on TB development.


2018 ◽  
Vol 15 (1) ◽  
pp. 31-43 ◽  
Author(s):  
Sayantan Nath ◽  
Sambuddha Das ◽  
Aditi Bhowmik ◽  
Sankar Kumar Ghosh ◽  
Yashmin Choudhury

Background:Studies pertaining to association of GSTM1 and GSTT1 null genotypes with risk of T2DM and its complications were often inconclusive, thus spurring the present study.Methods:Meta-analysis of 25 studies for evaluating the role of GSTM1/GSTT1 null polymorphisms in determining the risk for T2DM and 17 studies for evaluating the role of GSTM1/GSTT1 null polymorphisms in development of T2DM related complications were conducted.Results:Our study revealed an association between GSTM1 and GSTT1 null polymorphism with T2DM (GSTM1; OR=1.37;95% CI =1.10-1.70 and GSTT1; OR=1.29;95% CI =1.04-1.61) with an amplified risk of 2.02 fold for combined GSTM1-GSTT1 null genotypes. Furthermore, the GSTT1 null (OR=1.56;95%CI=1.38-1.77) and combined GSTM1-GSTT1 null genotypes (OR=1.91;95%CI=1.25- 2.94) increased the risk for development of T2DM related complications, but not the GSTM1 null genotype. Stratified analyses based on ethnicity revealed GSTM1 and GSTT1 null genotypes increase the risk for T2DM in both Caucasians and Asians, with Asians showing much higher risk of T2DM complications than Caucasians for the same. </P><P> Discussion: GSTM1, GSTT1 and combined GSTM1-GSTT1 null polymorphism may be associated with increased risk for T2DM; while GSTT1 and combined GSTM1-GSTT1 null polymorphism may increase the risk of subsequent development of T2DM complications with Asian population carrying an amplified risk for the polymorphism.Conclusion:Thus GSTM1 and GSTT1 null genotypes increases the risk for Type 2 diabetes mellitus alone, in combination or with regards to ethnicity.


Sign in / Sign up

Export Citation Format

Share Document