ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is distinguished by liver injury due to metabolic stress, identified by diffuse hepatocyte macrovascular fatty lesions [1]. The prevalence of NAFLD is rising yearly, with a worldwide incidence rate between 20% and 30% [2]. Complex hereditary variables, improper lipid metabolism, and insulin resistance are the key characteristics of the etiology of NAFLD [3]. The research has revealed that aberrant lipid metabolism in the liver can result in dysbacteriosis in the intestinal flora; abnormality of the flora eventually encourages lipid deposition in the liver. Additionally, there is mounting proof that NALFD is linked to abnormalities in the gut flora, particularly Helicobacter pylori (H, pylori) [4]. Gram-negative bacillus, termed H pylori, has colonized the deep layers of the gastric mucosa. [5]. The global infection rate for H pylori is about 50% or higher [6]. According to research, H pylori causes gastric cancer, gastrointestinal lymphoma, peptic ulcers, and chronic gastritis [7]. Additionally, some researchers indicate a connection between H pylori and liver cancers, diabetes, and improper lipid metabolism [8]. Some studies have discovered that infection by H pylori is one of the elements for NAFLD to progress and that getting rid of H pylori can partially stop the evolution of NAFLD [9].