Non-Alcoholic Steatohepatitis (NASH): An Update
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Diabetes, gut dysbiosis, hypercholesteremia, Non-alcoholic Steatohepatitis, obesity
Abstract
Non-alcoholic Steatohepatitis (NASH) is a globally rising, multifactorial disease which may be a result of obesity, diabetes (type-2), hypercholesteremia and gut dysbiosis. NASH is characterized by inflammation and fibrosis of liver tissues which further leads to hepatocellular carcinoma or liver failure. Patients with non-alcoholic fatty liver disease (NAFLD) show symptoms of NASH in which the fat accumulation in the liver exceeds 5-10%. Accumulation of this fat in the form of triglyceride in the hepatocytes is the key factor for the development of NASH. This may be caused due to increase in the flow of fatty acid and de novo lipogenesis. This abnormal retention of fat leads to lipotoxicity, which can cause apoptosis, necrosis, inflammation and an increase in oxidative stress. Since the pathological factors associated with NASH are unclear, the treatment to control the progression and management of the disease is cumbersome. Progress is being made in order to understand the cellular and molecular mechanisms associated with the pathogenesis of this condition. With studies reporting that NASH is the most common liver disease after hepatitis C, there is an increase in the demands for medical therapy and diagnosis of NASH. However, no treatment has been proven to be effective for long-term use. Gut dysbiosis, major pathways involved in NASH progression, experimental animal models and the current therapeutic strategies for NASH is discussed in the present review.
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References
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