الفهرس 
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Abstract
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on-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western industrialised countries and affects around 25% of the European population. The prevalence of NAFLD is increasing in parallel with the global increase in obesity and type 2 diabetes mellitus (T2DM).
NAFLD is histologically further divided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). NAFL is defined as the presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes. NASH is defined as the presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis.
All patients of NAFLD irrespective of the liver enzyme elevation should undergo a detailed physical examination and anthropometry including, height, weight, BMI, waist circumference, and waist–hip ratio for the assessment of overweight and central and overall obesity. These patients should be further evaluated with full liver function tests (LFTs) and for the presence of other components of metabolic syndrome namely hypertension, IGT, serum triglycerides, and HDL.
In addition, all patients should also be screened for viral markers including hepatitis B surface antigen (HBsAg) and antibodies to hepatitis C virus (anti-HCV). Further work-up should include also autoimmune markers, celiac disease work-up, serum iron profile, and serum ceruloplasmin should be done only in patients with elevated liver enzymes depending on the age of the patient.
In response to inflammatory cytokines and liver injury, collagen deposition occurs in the liver causing fibrosis. Noninvasive tests for fibrosis may decrease the need for liver biopsy in patients with nonalcoholic fatty liver disease. A commercially available combination of serologic markers of fibrosis has a sensitivity of 47% and specificity of 90% for detecting advanced fibrosis.
Adiponectin is an adipokine that impacts on the hepatic fat and glucose metabolism. It interacts with adiponectin receptor 56 (AdipoR1) and AdipoR2. AdipoR2 is predominantly expressed in hepatic tissue. Under normal conditions, adiponectin has antisteatotic, antiinflammatory and antifibrotic effects, which protect against the development of fatty liver disease.
Several studies in humans have demonstrated lower serum adiponectin levels in patients with NAFLD compared with healthy controls.
IGFs are central hormones involved in metabolic signaling, affecting glucose uptake, lipogenesis, glycogen storage, and suppression of protein degradation. IGF1 is necessary for normal insulin sensitivity, and impairment of IGF1 synthesis results in worsening of the state of insulin resistance.
The main functions of IGF system in liver physiology include the role of the system in organ development, growth and regeneration. At the cellular level, both IGFs (endocrine and autocrine/paracrine), as well as their receptors (IGF1R, IGF2R), regulate the cell cycle progression, proliferation and hepatocytes differentiation.
Concerning the role of the GH/IGF1 system in the pathogenesis of NAFLD/NASH, it has been reported that the decrease in the levels of the system components is closely associated with the progression of NAFLD. Low IGF1, and IGF1/IGFBP3 ratio may be associated with advanced hepatic fibrosis, while low levels of GH might have a role in hepatic steatosis in NAFLD.
The present study was designed to investigate the role of adiponectin and IGF 1 in NAFLD and NASH patients