Key result
Insulin resistance, free fatty acids, and oxidative stress are the primary pathophysiological drivers of nonalcoholic steatohepatitis (NASH), leading to hepatocellular injury and progressive fibrosis.
This review highlights insulin resistance, free fatty acid toxicity, and oxidative stress as the core mechanisms driving the progression of nonalcoholic steatohepatitis.
Nonalcoholic steatohepatitis (NASH) is a clinicopathological condition that comprises a wide spectrum of liver damage, ranging from steatohepatitis, advanced fibrosis and cirrhosis. NASH is the most common liver disease in the United States, with a high prevalence in the obese, type 2 diabetic population and metabolic syndrome. Although the pathophysiology of NASH remains to be clarified, insulin resistance, free fatty acids and oxidative stress are the most important causes. In this review article, I focused on insulin resistance, free fatty acids and oxidative stress as main causes of NASH, and described the outlines of the pathophysiology of NASH.
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Shiota et al. (2006) conducted a review in Nonalcoholic steatohepatitis (NASH). Insulin resistance, free fatty acids, and oxidative stress are the primary pathophysiological drivers of nonalcoholic steatohepatitis (NASH), leading to hepatocellular injury and progressive fibrosis.
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