Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. It is a progressive disorder involving a spectrum of conditions that include pure steatosis without inflammation, nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis. The key factor in the pathophysiology of NAFLD is insulin resistance that determines lipid accumulation in the hepatocytes, which may be followed by lipid peroxidation, production of reactive oxygen species and consequent inflammation. Recent studies suggest that the characteristics of the gut microbiota are altered in NAFLD, and also, that small intestinal bacterial overgrowth (SIBO) contributes to the pathogenesis of this condition. This review presents the chief findings from all the controlled studies that evaluated SIBO, gut permeability and endotoxemia in human NAFLD. We also discuss the possible mechanisms involving SIBO, lipid accumulation and development of NASH. The understanding of these mechanisms may allow the development of new targets for NASH treatment in the future.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is considered the most prevalent chronic liver disease in the western world [1]. It is usually associated with the metabolic syndrome (MS), and encompasses a spectrum of clinicopathological conditions that ranges from simple hepatic steatosis to hepatic steatosis associated with necroinflammatory lesions (nonalcoholic steatohepatitis (NASH)) with or without hepatic fibrosis that may progress to cirrhosis
NASH group: higher prevalence of small intestinal bacterial overgrowth (SIBO) (50% vs. 22%; p = 0.048); higher mean tumor necrosis factor (TNF)-α levels (p = 0.01)
The data described here support the notion that SIBO induces an immune imbalance leading to a state of chronic inflammation, mitochondrial dysfunction, hepatic fat accumulation and NASH
Summary
Nonalcoholic fatty liver disease (NAFLD) is considered the most prevalent chronic liver disease in the western world [1]. This excessive deposition of triglyceride in the liver leads to a shift from carbohydrates to FFA mitochondrial beta-oxidation, and may promote lipid peroxidation and accumulation of reactive oxygen species (ROS) in the hepatocytes These compounds produce a variety of cellular stimuli with subsequent inflammatory response, hepatocellular injury, and fibrosis [2,4]. Obese subjects present distinct microbiota composition with relative low proportion of Bacteroidetes and predominance of Firmicutes [7] This predominance has been associated with a propensity to develop NAFLD features, such as fasting hyperglycemia, hyperinsulinemia, hepatic steatosis, and increased expression of genes involved in de novo lipogenesis, independently of the presence of obesity, in animals models [8]. The suggested mechanisms to explain the role of SIBO in lipid accumulation and development of NASH are the focus of the present comprehensive review.
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