Abstract
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.
Highlights
Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of hepatic pathology consisting of simple steatosis, steatosis plus lotbular inflammation, steatosis plus balloning degeneration, and steatosis plus balloning degeneration plus Mallory bodies or fibrosis [1]
In patients the high frequency of D/D genotype but no association between necroinflammatory activity and fibrosis suggest that angiotensin converting enzyme (ACE) gene had no role in the development of fibrosis in non-alcoholic fatty liver disease, it is a component of general metabolic disorder
It was found that serum ACE levels were found to be increased approximately two times in people with DD allele of ACE gene and it was reported that increased serum angiotensin II levels in people with DD allele were associated with insulin resistance, systemic hypertension, atherosclerosis, coronary artery disease and diabetic nephropathy [7]
Summary
Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of hepatic pathology consisting of simple steatosis (type 1), steatosis plus lotbular inflammation (type 2), steatosis plus balloning degeneration (type 3), and steatosis plus balloning degeneration plus Mallory bodies or fibrosis (type 4) [1]. The role of the ACE gene I/D polymorphism as a risk factor has been investigated in several diseases [5]. The findings that angiotensin converting enzyme inhibitors (ACE-I) and AT-II receptor antagonists decrease hepatic fibrosis support the effects of angiotensin and its receptors on liver fibrosis [6]. It was found that serum ACE levels were found to be increased approximately two times in people with DD allele of ACE gene and it was reported that increased serum angiotensin II levels in people with DD allele were associated with insulin resistance, systemic hypertension, atherosclerosis, coronary artery disease and diabetic nephropathy [7]. In our study we aimed to investigate the role of polymorphism of ACE gene in NAFLD pathogenesis
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