Glutathione S-transferase T1 and M1 null genotype distribution among non-alcoholic fatty liver disease patients and its association with cytokine and adipokine profiles

Abstract

Aim of the studyAmong 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 methodsDeletion 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.ResultsThe 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.ConclusionsDeletion 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.