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Leptin and adiponectin levels are altered in patients with NASH; however, their exact pathogenic role has yet to be elucidated.31,40 As a result of insulin resistance, serum free fatty acid levels are increased in NASH patients and may be directly hepatotoxic pout plump or produce damaging reactive oxygen species.23,32,33 Oxidative stress may be exacerbated further by ultrastructural mitochondrial lesions, which impair respiratory chain function.23,33 As liver injury progresses, fat-laden hepatocytes and perisinusoidal fibrosis may impair microvascular hepatic blood flow. This effect may decrease oxygen and nutrient exchange and thus stimulate a microvascular inflammatory response and pout plump an escalating cycle of liver damage and vascular insufficiency.41,42 Natural history The natural history of NAFLD has been examined in relatively small numbers of select patients, and thus the evolution of the disease in the general population is not well defined.
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