Angiotensin-converting enzyme gene rs4343 polymorphism increases susceptibility to migraine.
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ABSTRACT:
SUBMITTER: Abedin-Do A
PROVIDER: S-EPMC6492685 | biostudies-literature | 2017 Aug
REPOSITORIES: biostudies-literature
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Angiotensin-converting enzyme gene rs4343 polymorphism increases susceptibility to migraine.
Abedin-Do Atieh A Pouriamanesh Sara S Kamaliyan Zeeba Z Mirfakhraie Reza R
CNS neuroscience & therapeutics 20170618 8
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Project description:Angiotensin-converting enzyme (ACE) plays a major role in blood pressure regulation and cardiovascular homeostasis. Contrary to the assumption that ACE levels are stable, circulating ACE has been shown to be altered in obesity and weight loss. We sought to examine effects of a high-saturated-fat (HF) diet on ACE within the NUtriGenomic Analysis in Twins (NUGAT) study. Forty-six healthy and nonobese twin pairs initially consumed a carbohydrate-rich, low-fat diet over a period of 6 weeks to standardize for nutritional behavior prior to the study, followed by 6 weeks of HF diet under isocaloric conditions. After 6 weeks of HF diet, circulating ACE concentrations increased by 15% (P=1.6×10-30), accompanied by an increased ACE gene expression in adipose tissue (P=3.8×10-6). Stratification by ACE rs4343, a proxy for the ACE insertion/deletion polymorphism (I/D), revealed that homozygous carriers (GG) of the variant had higher baseline ACE concentrations (P=7.5×10-8) and additionally showed a 2-fold increase in ACE concentrations in response to the HF diet as compared to non- or heterozygous carriers (AA/AG, P=2×10-6). GG carriers also responded with higher systolic blood pressure as compared to AA/AG carriers (P=0.008). The strong gene-diet interaction was confirmed in a second independent, cross-sectional cohort, the Metabolic Syndrome Berlin Potsdam (MeSyBePo) study. The HF-diet-induced increase of ACE serum concentrations reveals ACE to be a potential molecular link between dietary fat intake and hypertension and cardiovascular disease (CVD). The GG genotype of the ACE rs4343 polymorphism represents a robust nutrigenetic marker for an unfavorable response to high-saturated-fat diets. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01631123.
| S-EPMC5523633 | biostudies-literature
Project description:PurposeThis is the first cross-sectional study studying the changes in haematological indicators of the response to recombinant human erythropoietin (rHuEPO) therapy in chronic renal failure (CRF) patients on haemodialysis (HD) stratified according to ACE G2350A (rs4343) gene polymorphism.DesignAn observational cross-sectional study.SettingNephrology department and Biochemistry and molecular biology department, faculty of medicine, Cairo University.PatientsA total of 256 CRF patients on HD for at least six months (162 male and 103 female) and 160 healthy subjects (122 male and 38 female) were recruited in the current study after signing a consent form. ACE G2350A (rs4343) Insertion/Deletion (I/D) was tested, the association between ACE G2350A (RS4343) gene polymorphisms and patients response to rHuEpo was evaluated.ResultsACE G2350A (rs4343) I/D was the most prevalent genotype, while I/I genotype was the lowest prevalent among patient or control subjects included in the study. D allele is the most prevalent allele, either among patients or the control group. Hemoglobin (Hb) level in patients with I/I and Deletion/Deletion (D/D) genotype was significantly higher compared to those with I/D genotype (P = 0.012 and P = 0.005, respectively). Serum iron in the I/D genotype was significantly higher than those with either I/I or D/D genotype (P = 0.045 and P = 0.018, respectively). Angiotensin-converting enzyme (ACE) content, total leukocytic count (TLC), and soluble erythropoietin receptor (sEpoR) were independent predictors of Hb level. The ACE gene, TLC, and serum iron were the independent factors that may affect the Haematocrit (Hct) level. ACE G2350A (rs4343) gene polymorphisms may affect the HD patient's responses to rHuEPOs.ConclusionIn HD patients, screening for ACE G2350A (rs4343) gene polymorphisms before rHuEpo administration may help predict patient response.
| S-EPMC8408344 | biostudies-literature
Project description:Mild gestational hyperglycemia (MGH) is a very common complication of pregnancy that is characterized by intolerance to glucose. The association of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism to MGH has been previously reported. In this study, we evaluated the association between ACE polymorphism and the risk of MGH in a Saudi population. We conducted a case-control study in a population of 100 MGH patients and 100 control subjects. ACE gene polymorphism was analyzed by the novel approach of tetraprimer amplification refractory mutation system (ARMS)-polymerase chain reaction (PCR). The frequency of ACE polymorphism was not associated with either alleles or genotypes in MGH patients. Glucose concentration was found to be significantly associated with the MGH group. Our study suggests that ACE genotypes were not associated with ACE polymorphism in a Saudi population.
| S-EPMC4423719 | biostudies-literature
Project description:ObjectiveTo assess the polymorphism of angiotensin converting enzyme (ACE) in ischemic stroke in an Egyptian sample.MethodsOne hundred subjects (70 ischemic stroke patients, and 30 healthy controls) were included in case control cross sectional study during the period from January 2017 to January 2018, at Neurology Department, Menufia University Hospital, Shibin EL-Kom, Egypt. Patients underwent complete neurological assessment, national institute health stroke scale (NIHSS), and Toast classification. All subjects underwent genotyping of ACE gene polymorphism.ResultsThere are 42.9% from the patients versus 33.3% from controls showed geno typing of Insertion/Deletion (I/D) and Allele D is more frequent regarding I allele in ischemic stroke patients but this difference did not reach significant level to be risk factor. The I/D polymorphism was the predominant type in SVS and LVS while DD was the predominant type in cardio-embolic one. There were no significant differences between NIHSS in different ACE gene polymorphism.ConclusionIn spite of ACE genotyping differences among Egyptian ischemic stroke patients, we cannot consider it a predisposing factor to stroke occurrence or severity.
| S-EPMC8015476 | biostudies-literature
Project description:BackgroundThe angiotensin-converting enzyme (ACE) I/D polymorphism has been reported to be associated with Kawasaki disease (KD), but studies to date present conflicting results.ObjectivesThe aim of this study is to derive a more precise estimation of the association between the ACE I/D polymorphism and KD risk.MethodsPubMed, EMBASE, CNKI and Wangfang databases were retrievaled to identify for relevant studies from inception to May 2017. Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated using Stata 12.0 software.ResultsA total of 6 case-control studies comprising 634 patients and 458 controls were included in the meta-analysis, and we found a significant association between the ACE I/D polymorphism and KD risk (D vs I:OR = 0.81, 95%CI = 0.31-2.11;DD vs II: OR = 1.03, 95%CI = 0.42-2.54; DI vs II: OR = 1.44, 95%CI = 1.09-1.90; dominant model: OR = 1.43, 95%CI = 1.11-1.85; recessive model: OR = 1.21, 95%CI = 0.44-3.29 ). When stratified by sample size>200, this polymorphism is associated with an increased the risk of KD.ConclusionThe I/D polymorphism in the ACE gene may be associated with susceptibility to KD.
| S-EPMC5870280 | biostudies-literature
Project description:ObjectiveIt has yet to be determined whether genotyping at the angiotensin-converting enzyme (ACE) locus is predictive of blood pressure response to an ACE inhibitor.MethodsParticipants from the African American Study of Kidney Disease and Hypertension trial randomized to the ACE inhibitor ramipril (n = 347) were genotyped at three polymorphisms on ACE, just downstream from the ACE insertion/deletion polymorphism (Ins/Del): G12269A, C17888T, and G20037A. Time to reach target mean arterial pressure (</=107 mmHg) was analyzed by genotype and ACE haplotype using Kaplan-Meier survival curves and Cox proportional hazard models.ResultsIndividuals with a homozygous genotype at G12269A responded significantly faster than those with a heterozygous genotype; the adjusted (average number of medications and baseline mean arterial pressure) hazard ratio (homozygous compared to heterozygous genotype) was 1.86 (95% confidence limits 1.32-3.23; P < 0.001 for G12269A genotype). The adjusted hazard ratio for participants with homozygous ACE haplotypes compared to those heterozygous ACE haplotypes was 1.40 (1.13-1.75; P = 0.003 for haplotype). The ACE genotype effects were specific for ACE inhibition (i.e., not seen among those randomized to a calcium channel blocker), and were independent of population stratification.ConclusionsAfrican-Americans with a homozygous genotype at G12269A or homozygous ACE haplotypes responded to ramipril significantly faster than those with a heterozygous genotype or heterozygous haplotypes, suggesting that heterosis may be an important determinant of responsiveness to an ACE inhibitor. These associations may be a result of biological activity of this polymorphism, or of linkage disequilibrium with nearby variants such as the ACE Ins/Del, perhaps in the regulation of ACE splicing.
| S-EPMC2792638 | biostudies-literature
Project description:OBJECTIVES:The aim of the study was to evaluate the correlation between left ventricular hypertrophy and the gene polymorphism of angiotensin-converting enzyme (ACE) intron deletion (I/D) and ACE G2350A. METHODS:Information related to the sample size and genotype frequencies was extracted from each study. RESULTS:Our results found that the D allele (p = 0.0180) and DD genotype (p = 0.0110) of ACE I/D had a significant association with increasing the risk of left ventricular hypertrophy, whereas the I allele (p = 0.0180), but not II (p = 0.1660) and ID genotypes (p = 0.1430), was associated with decreasing the risk of left ventricular hypertrophy. On other hand, we found that the A allele (p = 0.0020) and GA genotype of ACE G2350A (p = 0.0070) had the correlation with increasing the risk of left ventricular hypertrophy. CONCLUSIONS:Our meta-analysis reveals that the D allele of ACE I/D and the A allele of ACE G2350A are associated with increasing the risk of left ventricular hypertrophy.
| S-EPMC6796625 | biostudies-literature
Project description:Background and purposeThe angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism has been studied as a genetic candidate for cerebral small vessel disease (CSVD). However, no previous study has evaluated the relationship between the ACE I/D polymorphism and cerebral microbleed (CMB), an important CSVD marker. We evaluated the association between ACE I/D polymorphisms and 2-year changes in CMBs.MethodsThe CHALLENGE (Comparison Study of Cilostazol and Aspirin on Changes in Volume of Cerebral Small Vessel Disease White Matter Changes) database was analyzed. Of 256 subjects, 186 participants who underwent a 2-year follow-up brain scan and ACE genotyping were included. Our analysis was conducted by dividing the ACE genotype into two groups (DD vs. ID/II) under the assumption of the recessive effects of the D allele. A linear mixed-effect model was used to compare the 2-year changes in the number of CMBs between the DD and combined ID/II genotypes.ResultsAmong 186 patients included in this study, 24 (12.9%) had the DD genotype, 91 (48.9%) had the ID genotype, and 71 (38.2%) had the II genotype. Baseline clinical characteristics and cerebral small vessel disease markers were not different between the two groups (DD vs. ID/II) except for the prevalence of hypertension (DD 66.7% vs. ID/II 84.6%; p = 0.04). A multivariate linear mixed-effects model showed that the DD carriers had a greater increase in total CMB counts than the ID/II carriers after adjusting for the baseline number of CMBs, age, sex, and hypertension (estimated mean of difference [standard error (SE)] = 1.33 [0.61]; p = 0.03). When we performed an analysis of cases divided into deep and lobar CMBs, only lobar CMBs were significantly different between the two groups (estimated mean of difference [SE] = 0.94 [0.42]; p = 0.02).ConclusionThe progression of CMBs over 2 years was greater in the ACE DD carriers compared with the combined II/ID carriers. The results of our study indicate a possible association between the ACE I/D polymorphism and CMB. A study with a larger sample size is needed to confirm this association.
| S-EPMC10602736 | biostudies-literature
Project description:ObjectiveThe angiotensin-converting enzyme gene is one of the most studied candidate genes related to atrial fibrillation. Among the polymorphisms of the angiotensin-converting enzyme gene, the 2350 G/A polymorphism (rs4343) is known to have the most significant effects on the plasma angiotensin-converting enzyme concentration. The aim of the present study was to investigate the association of the angiotensin-converting enzyme 2350 G/A polymorphism with atrial fibrillation in Han Chinese patients with essential hypertension.MethodsA total of 169 hypertensive patients were eligible for this study. Patients with atrial fibrillation (n = 75) were allocated to the atrial fibrillation group, and 94 subjects without atrial fibrillation were allocated to the control group. The PCR-based restriction fragment length polymorphism technique was used to assess the genotype frequencies.ResultsThe distributions of the angiotensin-converting enzyme 2350 G/A genotypes (GG, GA, and AA, respectively) were 40.43%, 41.49%, and 18.08% in the controls and 18.67%, 46.67%, and 34.66% in the atrial fibrillation subjects (p = 0.037). The frequency of the A allele in the atrial fibrillation group was significantly greater than in the control group (58.00% vs. 38.83%, p = 0.0007). Compared with the wild-type GG genotype, the GA and AA genotypes had an increased risk for atrial fibrillation. Additionally, atrial fibrillation patients with the AA genotype had greater left atrial dimensions than the patients with the GG or GA genotypes (p<0.01 and p<0.05, respectively).ConclusionsThe results obtained in this study indicate that the angiotensin-converting enzyme 2350 G/A polymorphism is associated with atrial fibrillation and that the A allele shows an increased risk for atrial fibrillation in Han Chinese patients with essential hypertension.
| S-EPMC3812555 | biostudies-literature
Project description:ObjectiveThis meta-analysis aims to explore the association between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and susceptibility to prostate cancer (PCa).MethodsWe searched studies related to ACE I/D polymorphism and susceptibility to PCa through PubMed, Web of Science, Embase, Cochrane Library, and Scopus databases from inception to June 1, 2022. Five gene models, including allelic, dominant, recessive, homozygote, and heterozygote models, were analyzed. The pooled odds ratio (OR) was calculated using Stata 15.0 software. Publication bias was judged by the funnel plot and Egger's test, with the robustness of the findings verified by sensitivity analysis.ResultsEight published articles (including ten studies) were identified. The pooled results showed that ACE I/D locus polymorphism was significantly correlated with the risk of PCa under all gene models except for the heterozygous model (D vs. I: OR= 1.58, 95% CI: 1.14-2.21; DD vs. DI+II: OR=1.68, 95% CI: 1.11-2.54; DD+DI vs. II: OR=1.76, 95% CI: 1.11-2.80; DI vs. II: OR= 1.44, 95% CI: 0.99-2.10; DD vs. II: OR= 2.12, 95% CI: 1.15-3.93). Subgroup analysis based on genotype frequencies in the control group meeting Hardy-Weinberg equilibrium showed statistically significant differences in all gene models. The funnel plot and Egger's test indicated no publication bias. The sensitivity analysis verified the robustness of the conclusions obtained in this meta-analysis.ConclusionACE I/D locus polymorphism correlates to PCa risk. Allele D, genotype DD+DI, and DD at the ACE I/D locus increase susceptibility to PCa and can therefore serve as a potential diagnostic and screening molecular marker for PCa patients.
| S-EPMC9635097 | biostudies-literature