Non-Alcoholic Fatty Liver Disease Is Associated with a Decreased Catalase (CAT) Level, CT Genotypes and the T Allele of the -262 C/T CAT Polymorphism.
Cells
; 12(18)2023 09 07.
Article
em En
| MEDLINE
| ID: mdl-37759451
BACKGROUND: It is well known that oxidative stress plays an important role in the development of non-alcoholic fatty liver disease (NAFLD). It has been suggested that an insufficient antioxidant defense system composed of antioxidant enzymes, including catalase (CAT) and nonenzymatic molecules, is a key factor triggering oxidative damage in the progression of liver disease. Therefore, the aim of our study was to assess whether the level of CAT and -262 C/T polymorphism in the promoter of CAT (rs1001179) are associated with NAFLD. METHODS: In total, 281 adults (152/129 female/male, aged 65.61 ± 10.44 years) were included in the study. The patients were assigned to an NAFLD group (n = 139) or a group without NAFLD (n = 142) based on the results of an ultrasound, the Hepatic Steatosis Index, and the Fatty Liver Index (FLI). CAT levels were determined using an ELISA test, and genomic DNA was extracted via the standard phenol/chloroform-based method and genotyped via RFLP-PCR. RESULTS: The CAT level was decreased in NAFLD patients (p < 0.001), and an ROC analysis revealed that a CAT level lower than 473.55 U/L significantly increases the risk of NAFLD. In turn, genotyping showed that the CT genotype and the T allele of -262 C/T CAT polymorphism elevate the risk of NAFLD. The diminished CAT level in the NAFLD group correlated with increased FLI, waist circumference and female gender. CONCLUSION: The obtained results support observations that oxidative damage associated with NAFLD may be the result of a decreased CAT level as a part of the antioxidant defense system.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Catalase
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Hepatopatia Gordurosa não Alcoólica
Tipo de estudo:
Risk_factors_studies
Limite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article