Abstract
Background and study aim: Hepatic steatosis reflects an imbalance between the uptake and synthesis of fatty acids by the liver and their oxidation and export. The mechanism of cell injury remains unclear. Transforming growth factor – beta 1 (TGF-β1) as a proinflammatory cytokine has become an important issue in the context of pathogenesis and progression of non alcoholic fatty liver disease (NAFLD). This study was planned to assess the value of TGF-β1 in different forms of NAFLD. Patients and methods:This study included 62 patients; 20 patients with benign steatosis (group 1), 20 patients with non alcoholic steatohepatitis (NASH) (group 2) and 22 patients with cirrhosis (group 3), as well as 7 healthy subjects who served as a control group. Each group was subclassified according to the presence of obesity, type 2 diabetes mellitus and hypertriglyceridemia. All participants were subjected to abdominal ultrasound, ultrasound guided needle liver biopsy and routine laboratory investigations e.g. complete blood picture, liver function tests, fasting and 2 hours postprandial blood glucose and serum triglycerides. Results : Serum TGF-β1 in the benign steatosis group was insignificantly different from the control group, while NASH and cirrhosis groups had significantly higher levels compared to control and benign steatosis groups (P<0.001). TGF-β1 in NASH group was significantly higher than in cirrhosis group (428.78 ± 117.15 vs 260.42 ± 110.22 ng/ml, P=0.032). In benign steatosis group, TGF-β1 was insignificantly different among subgroups. In NASH and cirrhotic patients, TGF-β1 was significantly higher in dyslipidemic subgroups. Conclusion : Serum level of TGF-β1 was higher in patients with severe forms of NAFLD (NASH and cirrhosis) than in patients with benign steatosis
Highlights
Non alcoholic fatty liver disease (NAFLD) consists of a spectrum of diseases including simple steatosis, non alcoholic steatohepatitis (NASH) and cirrhosis
The mechanism of cell injury in non alcoholic fatty liver disease (NAFLD) entails that excess fatty acids in the liver induces formation of free radicals, which cause lipid peroxidation and induce proinflammatory cytokines [1]
Of the cytokines secreted as a response to cell injury, transforming growth factor – beta 1 (TGF-β1) plays the dominant role in mediating fibrosis, through its contribution to the activation of stellate cells and their production of extracellular matrix proteins [7]
Summary
Non alcoholic fatty liver disease (NAFLD) consists of a spectrum of diseases including simple steatosis, non alcoholic steatohepatitis (NASH) and cirrhosis. Of the cytokines secreted as a response to cell injury, transforming growth factor – beta 1 (TGF-β1) plays the dominant role in mediating fibrosis, through its contribution to the activation of stellate cells and their production of extracellular matrix proteins [7]. TGF-β1 is the most abundant isoform of this family It has many actions in the liver including: fibrogenesis, growth inhibition (of normal hepatocytes and stellate cells), mitogenesis, pro-apoptosis and chemoattraction [9]. To our knowledge, only scanty reports have assessed the link between TGF- 1 and different pathological spectrum of NAFLD. This study was designed to assess the value of TGF-β1 in different forms of NAFLD
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