Abstract: | Aim of the study: Among the key genes involved in the development of non-alcoholic fatty liver disease (NAFLD) are genes encoding the synthesis of glutathione S-transferase (GST). Material and methods: Deletion polymorphism of GSTT1 and GSTM1 genes was investigated in 104 NAFLD patients and 45 healthy individuals. Biochemical blood analysis, tumor necrosis factor-α (TNF-α), interleukin-10, leptin and adiponectin plasma levels were studied. Results: The distribution of deletion vs. non-deletion genotypes of the GSTT1 gene in NAFLD patients was 18 (17.3%) vs. 86 (82.7%) patients and in healthy people it was 6 (13.3%) vs. 39 (86.7%) individuals. The genotype distribution of the GSTM1 gene was as follows: 52 (50.0%) NAFLD patients had null genotype vs. 52 patients (50.0%) with non-deletion genotype; in the control group - 23 (51.1%) vs. 22 (48.9%) individuals. Deletion of the GSTT1 gene in NAFLD patients was associated with twice as high (p = 0.01) TNF-α level in the blood as compared to patients with normal genotype. Higher concentration of leptin in blood by 37.1% (p = 0.04) was observed in patients with null genotype of the GSTM1 gene, as compared to those with normal genotype. Conclusions: Deletion polymorphism of GSTT1 and GSTM1 genes distribution among NAFLD patients did not differ as compared to healthy individuals. Null-genotype GSTT1 gene carriers were characterized by higher TNF-α concentration and null-genotype GSTM1 gene carriers were characterized by elevated leptin level as compared to normal genotype carriers. |