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Polymorphism C776G in the transcobalamin II gene and homocysteine, folate and vitamin B12 concentrations. Association with MTHFR C677T and A1298C and MTRR A66G polymorphisms in healthy children.
Thromb Res 2007; 119(5):571-7TR

Abstract

One of the etiologies of hyperhomocysteinemia is decreased vitamin B(12). Genetic variation in the transcobalamin II gene, the transporter of vitamin B(12) to the cells, may produce altered homocysteine levels. We determined transcobalamin II C776G polymorphism, homocysteine, folate and vitamin B(12) levels and analyzed the interactive effect with the methylenetetrahydrofolate reductase C677T and A1298C and methionine synthase reductase A66G polymorphisms in 207 healthy Brazilian children. The prevalence of GG genotype of transcobalamin II C776G polymorphism in this Brazilian population, a highly miscigeneous population was 12.5% and the statistical analysis showed that this population is in Hardy-Weinberg equilibrium, it could be considered representative of the general population. We observed a significant increase in homocysteine in the 776GG vs. 776CC genotype, corroborating the influence of age as a determinant of homocysteine in relation to this polymorphism. When we analyzed vitamin B(12) and its relationship with the C776G polymorphism, we found no significant differences. Only 776CG/66AA or 776GG/66AG genotypes presented a significant increase in homocysteine when compared with other groups. In the multivariate analysis, transcobalamin II C776G (CC/CG vs. GG), methylenetetrahydrofolate reductase C677T (CC/CT vs. TT), folate, gender and age presented statistical significance in relation to the homocysteine. These can be considered independent risk factors for hyperhomocysteinemia in this children group. Our results, if confirmed in other populations, highlight the necessity for investigation of the transcobalamin II C776G polymorphism in the research for hyperhomocysteinemia risk factors.

Authors+Show Affiliations

Hematology-Hemotherapy Center, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil. alessio@fcm.unicamp.brNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16820193

Citation

Aléssio, Ana C M., et al. "Polymorphism C776G in the Transcobalamin II Gene and Homocysteine, Folate and Vitamin B12 Concentrations. Association With MTHFR C677T and A1298C and MTRR A66G Polymorphisms in Healthy Children." Thrombosis Research, vol. 119, no. 5, 2007, pp. 571-7.
Aléssio AC, Höehr NF, Siqueira LH, et al. Polymorphism C776G in the transcobalamin II gene and homocysteine, folate and vitamin B12 concentrations. Association with MTHFR C677T and A1298C and MTRR A66G polymorphisms in healthy children. Thromb Res. 2007;119(5):571-7.
Aléssio, A. C., Höehr, N. F., Siqueira, L. H., Bydlowski, S. P., & Annichino-Bizzacchi, J. M. (2007). Polymorphism C776G in the transcobalamin II gene and homocysteine, folate and vitamin B12 concentrations. Association with MTHFR C677T and A1298C and MTRR A66G polymorphisms in healthy children. Thrombosis Research, 119(5), pp. 571-7.
Aléssio AC, et al. Polymorphism C776G in the Transcobalamin II Gene and Homocysteine, Folate and Vitamin B12 Concentrations. Association With MTHFR C677T and A1298C and MTRR A66G Polymorphisms in Healthy Children. Thromb Res. 2007;119(5):571-7. PubMed PMID: 16820193.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Polymorphism C776G in the transcobalamin II gene and homocysteine, folate and vitamin B12 concentrations. Association with MTHFR C677T and A1298C and MTRR A66G polymorphisms in healthy children. AU - Aléssio,Ana C M, AU - Höehr,Nelci F, AU - Siqueira,Lúcia H, AU - Bydlowski,Sérgio P, AU - Annichino-Bizzacchi,Joyce M, Y1 - 2006/07/03/ PY - 2005/11/18/received PY - 2006/05/10/revised PY - 2006/05/11/accepted PY - 2006/7/6/pubmed PY - 2007/12/12/medline PY - 2006/7/6/entrez SP - 571 EP - 7 JF - Thrombosis research JO - Thromb. Res. VL - 119 IS - 5 N2 - One of the etiologies of hyperhomocysteinemia is decreased vitamin B(12). Genetic variation in the transcobalamin II gene, the transporter of vitamin B(12) to the cells, may produce altered homocysteine levels. We determined transcobalamin II C776G polymorphism, homocysteine, folate and vitamin B(12) levels and analyzed the interactive effect with the methylenetetrahydrofolate reductase C677T and A1298C and methionine synthase reductase A66G polymorphisms in 207 healthy Brazilian children. The prevalence of GG genotype of transcobalamin II C776G polymorphism in this Brazilian population, a highly miscigeneous population was 12.5% and the statistical analysis showed that this population is in Hardy-Weinberg equilibrium, it could be considered representative of the general population. We observed a significant increase in homocysteine in the 776GG vs. 776CC genotype, corroborating the influence of age as a determinant of homocysteine in relation to this polymorphism. When we analyzed vitamin B(12) and its relationship with the C776G polymorphism, we found no significant differences. Only 776CG/66AA or 776GG/66AG genotypes presented a significant increase in homocysteine when compared with other groups. In the multivariate analysis, transcobalamin II C776G (CC/CG vs. GG), methylenetetrahydrofolate reductase C677T (CC/CT vs. TT), folate, gender and age presented statistical significance in relation to the homocysteine. These can be considered independent risk factors for hyperhomocysteinemia in this children group. Our results, if confirmed in other populations, highlight the necessity for investigation of the transcobalamin II C776G polymorphism in the research for hyperhomocysteinemia risk factors. SN - 0049-3848 UR - https://www.unboundmedicine.com/medline/citation/16820193/Polymorphism_C776G_in_the_transcobalamin_II_gene_and_homocysteine_folate_and_vitamin_B12_concentrations__Association_with_MTHFR_C677T_and_A1298C_and_MTRR_A66G_polymorphisms_in_healthy_children_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0049-3848(06)00190-3 DB - PRIME DP - Unbound Medicine ER -