Angiotensin Converting Enzyme Gene (I/D) Polymorphism and Nonalcoholic Fatty Liver Disease

Aim: Fibrosis is a finding showing that the process can be progressive in the spectrum of non-alcoholic fatty liver disease. Activated hepatic stellate cells cause fibrosis induced by angiotensin II. In this study the relation between ACE gene (I/D) polymorphism and steatosis, necroinflammation and fibrosis in liver were investigated.
Method: 29 females and 30 males (mean age: 53±10) whose necroinflammatorty activity and fibrosis scoring in liver biopsies were made according to Brunt classification were included in the study. According to the histopathological findings in liver biopsies patients with non-alcoholic fatty liver disease were determined and ACE gene (I/D) polymorphism was studied by using genomic DNA isolated from peripheral blood samples.
Result: In patient groups DD genotype frequency was 86.4%, ID genotype frequency was 5.1% and genotype II frequency 8.5%. In patient there was no significant relation between ACE gene (I/D) polymorphism, and necroinflammatory activity and fibrosis.
Conclusion: In patients the high frequency of D/D genotype but no association between necroinflammatory activity and fibrosis suggest that ACE gene had no role in the development of fibrosis in non-alcoholic fatty liver disease, however it is a component of general metabolic disorder.