MTHFR 677 CT/MTHFR 1298 CC genotypes are associated with increased risk of hypertension in Indians

Markan, Suchita; Sachdeva, M.P.; Sehrawat, Badan Singh; Kumari, Savita; Jain, Sanjay; Khullar, Madhu

doi:10.1007/s11010-007-9434-5

Cited by 75 publications

(52 citation statements)

References 38 publications

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“…Increased Hcy levels have been associated with low folate and vitamin B 12 levels. Asian Indians have low folate levels, probably due to their dietary habits; 46,47 however, we did not observe any correlation between folate, B 12 and change in Hcy levels in our subjects. We did not observe any change in folate or vitamin B 12 levels after AHT, thus the reduction in Hcy levels with ACE inhibitors or b-blockers in the present study does not appear to be influenced by these factors.…”

Section: Discussioncontrasting

confidence: 76%

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

et al. 2008

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Recent studies have shown that antihypertensive drugs like diuretics increase plasma homocysteine (Hcy) levels. However, the effect of other antihypertensive drugs on plasma Hcy levels has not been tested extensively. The aim of present study was to investigate the effect of antihypertensive therapy (AHT) on Hcy levels in essential hypertensive subjects. A case-control study of 273 patients with essential hypertension (EH) and 103 normotensive controls was undertaken. Plasma Hcy levels were measured before and after 6 weeks of AHT. The genotyping of MTHFR C677T polymorphism was performed by polymerase chain reaction-restriction fragment length polymorphism. Angiotensin-converting enzyme (ACE) inhibitors and b-blockers significantly decreased and hydrochlorothiazides significantly increased the plasma Hcy levels in hypertensive patients (Po0.05). No significant association between MTHFR C677T genotypes and changes in Hcy levels in response to antihypertensive was observed in EH patients. The decrease in Hcy induced by b-blockers and ACE inhibitors observed in our study may be due to the improvement of endothelial function along with improved renal function. Thus, our results suggest that ACE inhibitors and b-blockers may provide additional beneficial therapeutic effects to the EH patients by decreasing Hcy levels.

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Section: Discussioncontrasting

confidence: 76%

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

et al. 2008

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“…In the past decade, genome-wide association studies have identified several genetic loci associated with BP variation in European populations, including one near the gene encoding the folate metabolising enzyme MTHFR (84)(85)(86) . This finding was also replicated in non-European cohorts including Chinese, Japanese, Indian and US populations (87)(88)(89)(90) .…”

Section: Novel Role Of Mthfr Genotype and Blood Pressuresupporting

confidence: 54%

Riboflavin status, MTHFR genotype and blood pressure: current evidence and implications for personalised nutrition

et al. 2016

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Clinical deficiency of the B-vitamin riboflavin (vitamin B 2 ) is largely confined to developing countries; however accumulating evidence indicates that suboptimal riboflavin status is a widespread problem across the developed world. Few international data are available on riboflavin status as measured by the functional biomarker, erythrocyte glutathione reductase activation coefficient, considered to be the gold standard index. One important role of riboflavin in the form of flavin dinucleotide is as a co-factor for the folate-metabolising enzyme methylenetetrahydrofolate reductase (MTHFR). Homozygosity for the common C677T polymorphism in MTHFR, affecting over 10 % of the UK and Irish populations and up to 32 % of other populations worldwide, has been associated with an increased risk of CVD, and more recently with hypertension. This review will explore available studies reporting riboflavin status worldwide, the interaction of riboflavin with the MTHFR C677T polymorphism and the potential role of riboflavin in personalised nutrition. Evidence is accumulating for a novel role of riboflavin as an important modulator of blood pressure (BP) specifically in individuals with the MTHFR 677TT genotype, with results from a number of recent randomised controlled trials demonstrating that riboflavin supplementation can significantly reduce systolic BP by 5-13 mmHg in these genetically at risk adults. Studies are however required to investigate the BP-lowering effect of riboflavin in different populations and in response to doses higher than 1·6 mg/d. Furthermore, work focusing on the translation of this research to health professionals and patients is also required.Riboflavin: Methylenetetrahydrofolate reductase: MTHFR C677T: Blood pressure:Personalised nutrition Riboflavin (vitamin B 2 ) is a water-soluble B-vitamin defined chemically as 7,8-dimethyl-10-1′-D-ribityl isoalloxazine. It acts as a precursor for FMN and FAD (1) . Clinical riboflavin deficiency is not generally considered to be a problem in the developed world but in recent years evidence has shown that sub-optimal status may be more widespread than generally perceived based on studies reporting the functional biomarker, erythrocyte glutathione reductase activation coefficient (EGRac) generally considered as the gold standard index of status. Few international data are however available based on EGRac and reports on riboflavin status are more commonly based solely on dietary intake data. Although riboflavin is required for numerous metabolic reactions its role (in the form of FAD) as a cofactor for the folatemetabolising enzyme, methylenetetrahydrofolate reductase (MTHFR) has recently received particular attention. Homozygosity (MTHFR 677TT genotype) for a common polymorphism in MTHFR, affecting over 10 % of the UK and Irish populations and up to 32 % of other populations worldwide (2) , has been associated with an increased risk of CVD (3) and more recently with hypertension (4) . Emerging evidence from intervention trials supports a novel role for riboflav...

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“…It was reported that MTHFR 677 CT genotype and MTHFR 677T allele are associated with an increased risk of hypertension (Markan et al 2007). In a metaanalysis, it was stated that the C677T polymorphism is associated with hypertension and this polymorphism is an independent risk factor for hypertension (Qian et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Is there any genetic predisposition of MMP-9 gene C1562T and MTHFR gene C677T polymorphisms with essential hypertension?

et al. 2013

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The current study was conducted to determine whether there is a relation between hypertension and two different polymorphisms, including C1562T of the Matrix metalloproteinase-9 (MMP-9) gene and C677T of the methylenetetrahydrofolate reductase (MTHFR) gene. Genomic DNA obtained from 224 persons (125 patients with hypertension and 99 healthy controls) were used in the study. Polymorphisms were determined by using polymerase chain reaction-restriction fragment length polymorphism and electrophoresis. The results were statistically analyzed and were found to be statistically significant. The frequencies of the C1562T genotypes were found to be, in controls CC 75.8 % and CT 24.2 % and in patients CC 71.2 %, and CT 28.8 %. The frequencies of C677T genotype were found to be, in controls CC 56.6 %, CT 38.4 and TT 5.1 % in controls and in patients CC 52 %, CT 30.4 % and TT 17.6 %. In conclusion, we may suggest that there is no relation between the essential hypertension and C1562T polymorphism of MMP-9 gene; on the other hand C677T polymorphism (genotype TT) of MTHFR gene can be regarded as a genetic indicator for the development of essential hypertension.

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MTHFR 677 CT/MTHFR 1298 CC genotypes are associated with increased risk of hypertension in Indians

Cited by 75 publications

References 38 publications

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

Riboflavin status, MTHFR genotype and blood pressure: current evidence and implications for personalised nutrition

Is there any genetic predisposition of MMP-9 gene C1562T and MTHFR gene C677T polymorphisms with essential hypertension?

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