Introduction:

nonalcoholic fatty liver disease (NAFLD) is a public health problem associated with the metabolic syndrome; its pathogenesis implies the start of a complex biochemical signaling cascade and its continuous stimulation could consolidate a fibrogenesis process in the tissue. The aim of the study was to analyze expression of genes involved in liver damage in the initial processes of the lesion in patients with NAFLD or with risk factors related to this pathology, in search of molecular biomarkers useful to clinical practice such as TGF-|31, COL1A2 and MMP20.

Methodology:

cross-sectional analytical study. Epidemiological, biochemical, and gene expression characteristics of TGF-|31, COL1A2 and MMP20 in liver tissue in individuals with risk factors for NAFLD were studied.

Results:

83 participants with risk factors associated to NAFLD were included; 22 individuals (26.5%) were diagnosed with NAFLD by ultrasonography. The risk factors found were hypertension (50.6%), obesity (49.4%), diabetes mellitus (34.9%) and dyslipidemia (21.7%). Dyslipidemia was significantly associated with the risk of developing NAFLD (OR = 4; p = 0.011). Significant differences were found for total cholesterol (p <0.05); and a gene expression of TGF-P1 (with NAFLD p <0.0001 and without NAFLD p <0.0001 versus control) and COL1A2 (with NAFLD p = 0.002 and without NAFLD p = 0.955 versus control) with a pattern of increasing expression at higher degree of liver injury.

Conclusion:

to conclude, we suggest activation of the signaling pathways that lead to fibrogenesis in individuals with risk factors for NAFLD, and much more accentuated in patients with NAFLD.