The serum parameters assay showed that the concentrations of MTHFR (476.57 vs. 395.27), DHFR (45.056 vs. 38.952), LPL (50.408 vs. 48.677), HCY (4.354 vs. 3.836), LEP (9.951 vs. 8.673), and IGF2 (1209.4 vs. 1027.7) in offspring serum of the FD group were significantly higher than those of the normal folate (NF) group ( P < 0.01).
The most important result of this study was that maternal C677C MTHFR gene polymorphisms are significant risk factors in for ADHD, and we argue that children with ADHD are exposed to folate deficiency, even if their mothers received a sufficient amount of folate during pregnancy.
Finally, the model simulations indicate that the 5fTHF futile cycle dampens the stochastic noise in FOCM that results from both folate deficiency and a common variant in the methylenetetrahydrofolate reductase (MTHFR) gene.
The serum parameters assay showed that the concentrations of MTHFR (476.57 vs. 395.27), DHFR (45.056 vs. 38.952), LPL (50.408 vs. 48.677), HCY (4.354 vs. 3.836), LEP (9.951 vs. 8.673), and IGF2 (1209.4 vs. 1027.7) in offspring serum of the FD group were significantly higher than those of the normal folate (NF) group ( P < 0.01).
Positive findings were of an elevated level of homocysteine as a result of vitamin B12 and folic acid deficiency as well as a genetic mutation in the MTHFR gene (encoding MTHFR enzyme which is vital in normal homocysteine metabolism).
Computational simulations indicate that the MTHFRC677T polymorphism and folate deficiency interact to increase the stochastic behavior of the FOCM network, with the greatest instability observed for reactions catalyzed by serine hydroxymethyltransferase (SHMT).
Among these three factors, folate deficiency had the greatest contribution to the serum tHcy concentration, followed by (in order of decreasing effect) MTHFRC677T and vitamin B12 deficiency.
Response of MiRNA-22-3p and MiRNA-149-5p to Folate Deficiency and the Differential Regulation of MTHFR Expression in Normal and Cancerous Human Hepatocytes.
This study suggests that Egyptian β-TM patients with MTHFR 677TT genotype could be at increasing risk of developing Hhcy particularly with folate deficiency.
Folate deficiency and methylenetetrahydrofolate reductase (MTHFR) as an important enzyme of folate and methionine metabolism are considered crucial for DNA synthesis and methylation.
Our results showed that MTHFR 677TT and MTR 2756AG + GG were independently associated with a higher risk of folate deficiency (TT vs. CC + CT, p < 0.001 and AG + GG vs. AA p = 0.030, respectively).
The common polymorphisms of the MTHFR (C677T and A1298C), MTRR (A66G), and MTR (A2756G) enzymes are well documented as folate deficiency-related disorders, but their roles have not been examined in acromegalic patients.
Multivariate analysis revealed associations of baseline folate deficiency with low counts at day 14 (p = 0.001) and MTHFR 1298 mutations with mucositis (p = 0.02).
Among controls the known effect of MTHFR 677T on plasma total homocysteine was more pronounced in men than in women (p<0.00004 for genotype-sex interaction) suggesting that in Poland folate deficiency is more prevalent in males.
Folate deficiency and the methylenetetrahydrofolate reductase (MTHFR) 677C>T polymorphism have been linked to negative symptoms in schizophrenia both independently and synergistically.
Folate deficiency due to the methylenetetrahydrofolate reductase (MTHFR) and methionine synthase (MS) variants leads to carcinogenesis by affecting DNA synthesis, repair, and methylation.
To verify the cytotoxic effects of folate deficiency on cells with different MTHFRC677T genotypes, 15 human peripheral lymphocyte cases with different MTHFR C677T genotypes were cultured in folic acid (FA)-deficient and -sufficient media for 9 days.
Folate deficiency and the presence of the 677C > T (CT) polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene have been implicated in the causation of malformations in the fetus (particularly cleft lip and palate and neural tube defects).
The C677T mutation of the methylenetetrahydrofolate reductase gene may induce hyperhomocysteinemia and could slightly increase the risk of arterial or venous thrombosis and pregnancy loss in individuals with folic acid deficiency.