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IL-17A, MCP-1, CCR-2, and ABCA1 polymorphisms in children with non-alcoholic fatty liver disease
Ulas Emre Akbulut1, Hamdi Cihan Emeksiz2, Senol Citli3
1University of Health Sciences, Antalya Education and Research Hospital, Department of Pediatric Gastroenterology Hepatology and Nutrition, Antalya, Turkey.
Insights
Genetic variations in IL-17A may contribute to non-alcoholic fatty liver disease (NAFLD) in obese children. This study found a link between the IL-17A A-allele and NAFLD in Turkish children, suggesting a potential genetic predisposition.
Area of Science:
- Pediatric Endocrinology
- Hepatology
- Genetics
Background:
- Childhood obesity epidemic drives rising non-alcoholic fatty liver disease (NAFLD) prevalence.
- NAFLD is associated with obesity, sedentary lifestyles, and genetic factors.
- Understanding genetic predispositions is crucial for NAFLD management in children.
Purpose of the Study:
- Investigate gene polymorphisms in obese Turkish children with NAFLD.
- Specifically examine MCP-1, CCR-2, ABCA1, and IL-17A variants.
- Determine potential genetic associations with NAFLD development.
Main Methods:
- Recruited 186 obese children (10-17 years), including 101 with NAFLD.
- Collected anthropometric data, biochemical markers (liver panel, lipids), and performed liver ultrasounds.
- Genotyped four specific gene variants: MCP-1, CCR-2, ABCA1, and IL-17A.
Main Results:
- No significant differences in BMI, waist/hip ratio, or body fat between groups.
- Elevated ALT, AST, and GGT levels in the NAFLD group.
- The A-allele of IL-17A (-197 G/A) (rs2275913) showed a significant association with NAFLD (OR 2.05, p=0.02).
Conclusions:
- Suggests a potential association between IL-17A (-197 G/A) polymorphism and NAFLD in obese Turkish children.
- Highlights the role of genetic variations in pediatric NAFLD.
- Further research needed to confirm the role of IL-17A in NAFLD pathogenesis.
Objective:
The prevalence of non-alcoholic fatty liver disease in children has risen significantly, owing to the worldwide childhood obesity epidemic in the last two decades. Non-alcoholic fatty liver disease is closely linked to sedentary lifestyle, increased body mass index, and visceral adiposity. In addition, individual genetic variations also have a role in the development and progression of non-alcoholic fatty liver disease. The aim of this study was to investigate the gene polymorphisms of MCP-1 (-2518 A/G) (rs1024611), CCR-2 (190 G/A) (rs1799864), ABCA1 (883 G/A) (rs4149313), and IL-17A (-197 G/A) (rs2275913) in obese Turkish children with non-alcoholic fatty liver disease.
Methods:
The study recruited 186 obese children aged 10-17 years, including 101 children with non-alcoholic fatty liver disease and 85 children without non-alcoholic fatty liver disease. Anthropometric measurements, insulin resistance, a liver panel, a lipid profile, liver ultrasound examination, and genotyping of the four variants were performed.
Results:
No difference was found between the groups in respect to age and gender, body mass index, waist/hip ratio, or body fat ratio. In addition to the elevated ALT levels, AST and GGT levels were found significantly higher in the non-alcoholic fatty liver disease group compared to the non non-alcoholic fatty liver disease group (p<0.05). The A-allele of IL-17A (-197 G/A) (rs2275913) was associated with non-alcoholic fatty liver disease (odds ratio [OR] 2.05, 95% confidence interval: 1.12-3.77, p=0.02).
Conclusions:
The findings of this study suggest that there may be an association between IL-17A (-197 G/A) (rs2275913) polymorphism and non-alcoholic fatty liver disease development in obese Turkish children.
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