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CD36 genetic variation, fat intake and liver fibrosis in chronic hepatitis C virus infection
Omar Ramos-Lopez1, Sonia Roman1, Erika Martinez-Lopez1
1Omar Ramos-Lopez, Sonia Roman, Erika Martinez-Lopez, Nora A Fierro, Karina Gonzalez-Aldaco, Alexis Jose-Abrego, Arturo Panduro, Department of Molecular Biology in Medicine, Civil Hospital of Guadalajara "Fray Antonio Alcalde", Guadalajara, Jalisco 44280, Mexico.
Insights
The CD36 AA genotype is linked to increased fat consumption and advanced liver fibrosis in chronic hepatitis C patients. This genetic variation may influence dietary habits and disease progression.
Area of Science:
- Genetics
- Hepatology
- Nutritional Science
Background:
- Chronic hepatitis C (CHC) is a significant cause of liver disease.
- Dietary factors and genetic predispositions play roles in CHC progression.
- The CD36 gene is involved in lipid metabolism and immune responses.
Purpose of the Study:
- To investigate the association between the CD36 polymorphism (rs1761667) and dietary intake in CHC patients.
- To determine the relationship between this CD36 variant and the severity of liver fibrosis (LF) in CHC.
- To explore potential links between genotype, diet, and liver health outcomes.
Main Methods:
- Seventy-three CHC patients were genotyped for the CD36 polymorphism (rs1761667) using real-time PCR.
- Dietary intake was assessed via three-day food records, focusing on macronutrients.
- Liver fibrosis was evaluated using transient elastography (Fibroscan) and the APRI score.
Main Results:
- The CD36 AA genotype was more prevalent (30.1%) and associated with higher caloric intake from total fat and saturated fatty acids.
- AA genotype carriers exhibited higher aspartate aminotransferase (AST) levels.
- The AA genotype was significantly linked to advanced liver fibrosis (F3-F4) compared to other genotypes.
Conclusions:
- The CD36 (rs1761667) AA genotype is associated with increased dietary fat intake in CHC patients.
- This genotype is also linked to a higher prevalence of advanced liver fibrosis.
- Findings suggest a potential role for CD36 genotype in modulating diet-related liver disease progression in CHC.
Aim:
To analyze the association of the CD36 polymorphism (rs1761667) with dietary intake and liver fibrosis (LF) in chronic hepatitis C (CHC) patients.
Methods:
In this study, 73 patients with CHC were recruited. The CD36 genotype (G > A) was determined by a TaqMan real-time PCR system. Dietary assessment was carried out using a three-day food record to register the daily intake of macronutrients. Serum lipids and liver enzymes were measured by a dry chemistry assay. LF evaluated by transient elastography (Fibroscan(®)) and APRI score was classified as mild LF (F1-F2) and advanced LF (F3-F4).
Results:
Overall, the CD36 genotypic frequencies were AA (30.1%), AG (54.8%), and GG (15.1%), whereas the allelic A and G frequencies were 57.5% and 42.5%, respectively. CHC patients who were carriers of the CD36 AA genotype had a higher intake of calories attributable to total fat and saturated fatty acids than those with the non-AA genotypes. Additionally, aspartate aminotransferase (AST) serum values were higher in AA genotype carriers compared to non-AA carriers (91.7 IU/L vs 69.8 IU/L, P = 0.02). Moreover, the AA genotype was associated with an increase of 30.23 IU/L of AST (β = 30.23, 95%CI: 9.0-51.46, P = 0.006). Likewise, the AA genotype was associated with advanced LF compared to the AG (OR = 3.60, 95%CI: 1.16-11.15, P = 0.02) or AG + GG genotypes (OR = 3.52, 95%CI: 1.18-10.45, P = 0.02).
Conclusion:
This study suggests that the CD36 (rs1761667) AA genotype is associated with higher fat intake and more instances of advanced LF in CHC patients.
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