Author(s): Nikhil D Patel
Abstract
Nonalcoholic fatty liver disease (NAFLD), hepatic manifestation of metabolic syndrome is now the commonest chronic liver disease due to rising obesity and diabetes. NAFLD progresses from simple steatosis (NAFL) to steatohepatitis (NASH) and cirrhosis. In presence of suitable genetic and environmental factors (diet/physical activity/ gut dysbiosis), insulin resistance (IR) and obesity results in adipose dysfunction, which triggers proinflammatory response, decreased lipolysis, increased de-novo lipogenesis and further increased IR. These occasions increment free unsaturated fat (FFA) motion to liver, which prompts triglyceride gathering (NAFL).Toxic levels of FFA in liver trigger increased β-oxidation and mitochondrial dysfunction (MD). Obesity, homocysteine and environmental factors trigger endoplasmic reticulum stress (ERS). MD and ERS result in reactive oxygen species (ROS) production. ROS activates antioxidant mechanisms (consisting of enzymes like Superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione transferase; and non-enzymes like vitamin A, C, E, β-carotene and glutathione) which scavenges them, but over production of ROS results in depletion of antioxidants. Homocysteine adds to ROS production and suppresses antioxidants.
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