الفهرس 
Non-alcoholic fatty liver diseaseOnly 14 pages are availabe for public view
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Abstract
Nonalcoholic fatty liver disease (NAFLD), is presently the most prevalent liver disease. NAFLD is portrayed by the deposition of fats in the hepatocytes that ranges from simple hepatosteatosis to nonalcoholic steatohepatitis, fibrosis, cirrhosis, as well as hepatocellular carcinoma (Henao-Mejia, et al; 2012, Kolodziejczyk, et al; 2019). Currently, NAFLD is becoming a global health concern which accounts for 25% prevalence worldwide with more than 30% prevalence projected among adults by 2030, due to the dominance of obesity, unhealthy dietary patterns and sedentary lifestyle patterns (Delzenne, et al; 2015, Estes, et al; 2018). Actually, the underlying precise mechanisms of NAFLD pathogenesis have just begun to be understood. The classic “multiple hit” theory states that lipid accumulation initiates hepatic steatosis and subsequently triggers multiple insults acting together (hormones/adipokines from adipose tissue, inflammation, deregulated fat metabolism, lipotoxicity, oxidative stress, mitochondrial dysfunction, and genetic and epigenetic factors), ultimately inducing NASH and cirrhosis (Delzenne, et al; 2015). In the recent decades, many studies have highlighted multiple risk factors of NAFLD, including gut microbiota dysbiosis, environmental, genetic and metabolic factors, unhealthy diet, insulin resistance (IR), as well as host-derived features like age, ethnicity, gender, antibiotic use, oxidative stress, inflammatory states and lifestyle. All these factors significantly contribute to NAFLD and hepatic steatosis and several molecular pathways have been identified in the progression of NAFLD (Knight, et al; 2017, Vallianou, et al; 2019). Among these abnormal conditions, alteration of gut microbial populations has been recognized as the most common risk factor for NAFLD, obesity and diabetes (Jia and Rajani, et al; 2018, Amabebe, et al; 2020).