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function and adipocytokine release from adipose tissue). Inadequateness in resembling either the liverpathology or the physiological alterations in experimental models of NAFLD will make it difficult totranslate results found in such laboratory model systems to the clinical situation and subsequently thedevelopment of therapeutic or prevention strategies of the disease. Specifically, an appropriate animalmodel of NAFLD should display not only steatosis, but also inflammation, liver cell injury (e.g.,ballooning of hepatocytes) and should, if long enough extended, also progress to fibrosis. Furthermore,the model should also display metabolic abnormalities like overweight, insulin resistance, impaired
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