MTHFR 677C/T and 1298A/C mutations and non-alcoholic fatty liver disease

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dc.authoridYALCIN, Kadir Serkan/0000-0002-8028-1070;
dc.contributor.authorKasapoglu, Benan
dc.contributor.authorTurkay, Cansel
dc.contributor.authorYalcin, Kadir Serkan
dc.contributor.authorKosar, Ali
dc.contributor.authorBozkurt, Alper
dc.date.accessioned2025-10-24T18:10:14Z
dc.date.available2025-10-24T18:10:14Z
dc.date.issued2015
dc.departmentMalatya Turgut Özal Üniversitesi
dc.description.abstractCommon genetic mutations encountered in folate metabolism may result in increased homocysteine (Hcy) levels. It has been reported that increased serum Hcy levels may affect the intracellular fat metabolism and may cause enhanced fatty infiltration in the liver resulting in non-alcoholic fatty liver disease (NAFLD). In total, 150 patients diagnosed with FLD by ultrasound examination and 136 healthy control patients that do not have any fatty infiltration in the liver were included in the study. Patients were grouped as mild (n=88), moderate (n=38) or severe (n=24) according to the stage of fatty liver in ultrasound. Serum liver function tests, Hcy, folic acid and vitamin B12 levels of the patients were studied. The genetic MTHFR C677T and A1298C polymorphisms of the patients were also evaluated. Although there was no significant difference in vitamin B12 and folic acid levels, in the severe group, Hcy levels were significantly higher than that of control and mild groups (p<0.001). By contrast, there was no significant difference in heterozygote MTHFR 677C/T and 1298A/C mutations, both MTHFR 677C/T and MTHFR 1298A/C mutations were more common in NAFLD groups compared with the control patients (p<0.001). We have determined increased Hcy levels and increased prevalence of homozygote MTHFR 677C/T and MTHFR 1298A/C mutations in patients with NAFLD compared with healthy controls. Larger studies are warranted to clarify the etiological role of the MTHFR mutations and Hcy levels in FLD.
dc.identifier.doi10.7861/clinmedicine.15-3-248
dc.identifier.endpage251
dc.identifier.issn1470-2118
dc.identifier.issn1473-4893
dc.identifier.issue3
dc.identifier.pmid26031974
dc.identifier.scopus2-s2.0-84941107934
dc.identifier.scopusqualityQ1
dc.identifier.startpage248
dc.identifier.urihttps://doi.org/10.7861/clinmedicine.15-3-248
dc.identifier.urihttps://hdl.handle.net/20.500.12899/4059
dc.identifier.volume15
dc.identifier.wosWOS:000355894600009
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherRoy Coll Phys London Editorial Office
dc.relation.ispartofClinical Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20251023
dc.subjectMTHFR mutations; homocysteine; fatty liver disease
dc.titleMTHFR 677C/T and 1298A/C mutations and non-alcoholic fatty liver disease
dc.typeArticle

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