Non-alcoholic fatty liver disease (NAFLD) is considered an important and economically significant public health problem, its progression can result in development of cirrhosis and hepatocellular carcinoma. Over the past two decades, NAFLD became the most widespread liver disease worldwide, affecting 25 % of the adult population globally with a range of 13.5 % in Africa, 30.4 % in South America and 31.8 % in the Middle East. NAFLD is a multifactorial disease, its onset results from the interaction of genetic predisposition and metabolic, inflammatory and environmental factors. The intestinal microbiome dysregulation, directly associated with the NAFLD development, plays the main role. The quantitative and qualitive microbiome composition may be affected by nutrition that results in dysbiosis, a diet rich in saturated fats, animal products and fructose. The species diversity of intestinal bacteria affects the absorption of both macro- and micronutrients, initiating many pathways that contribute to the accumulation of fat in the liver and trigger inflammatory cascades that provoke liver damage. The mechanisms of NAFLD development, associated with intestinal dysbiosis, include bacterial overgrowth syndrome, synthesis of endogenous ethanol and the development of endotoxinemia. In addition, they include dysregulation of short-chain fatty acids and branched-chain amino acids. Excess or lack of nutrients from food, in particular, of fructose and choline, also associated with the development of non-alcoholic fatty liver disease through gut microbiota. Debatable is a question about effects of intestinal dysbiosis on the progression of non-alcoholic fatty liver disease. The review presents discussion of the relationship between gut microbiota and other risk factors for the NAFLD progression, as well as the analysis of the role of intestinal dysbiosis in its pathogenesis.