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These compounds generate a variety of cellular stimulations with subsequent inflammatory response, which has been recognized as the causal factor of NASH/fibrosis (second causative step) [, ].. Introduction Over the last decades, obesity has become a global epidemic and an important public health problem in many countries [].

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In spite of growing knowledge, several aspects of NAFLD pathogenesis are still unknown.. We investigated the effects of a simple carbohydrate-rich diet on the development of obesity-related NAFLD and the impact of physical training on the metabolic abnormalities associated with this disorder. Product code for medal of honor warfighter originals

Excessive deposition of fat in adipocytes and muscles determines insulin resistance with subsequent accumulation of fat in the liver [], which, in turn, increases the rate of mitochondrial beta-oxidation of fatty acids and ketogenesis that can promote lipid peroxidation and accumulation of reactive oxygen species (ROS) in the hepatocytes [, ].. This condition is largely due to excessive consumption of saturated fats and simple sugars [, ], which, associated with sedentarism, represent the modern lifestyle [].. At the end of each experimental period (5, 10, 20, and 30 weeks), 6 animals from each group were sacrificed for blood tests and liver histology and immunohistochemistry.. Rats that underwent physical training showed increased high-density lipoprotein- (HDL-) cholesterol levels.. NAFLD encompasses a spectrum of increasingly severe clinicopathological conditions ranging from fatty liver to steatohepatitis (NASH) with or without hepatic fibrosis/cirrhosis.

From weeks 25 to 30, 6 animals from each group underwent physical training The experimental group animals developed obesity and NAFLD, characterized histopathologically by steatosis and hepatocellular ballooning, clinically by increased thoracic circumference and body mass index associated with hyperleptinemia, and metabolically by hyperglycemia, hyperinsulinemia, hypertriglyceridemia, increased levels of very low-density lipoprotein- (VLDL-) cholesterol, depletion of the antioxidants liver enzymes superoxide dismutase and catalase, and increased hepatic levels of malondialdehyde, an oxidative stress marker.. In conclusion, a sucrose-rich diet induced obesity, insulin resistance, oxidative stress, and NAFLD in rats.. Manual De Cardiologia VeterinariaThe pathogenesis of nonalcoholic fatty liver disease (NAFLD) is not fully understood, and experimental models are an alternative to study this issue.. Recent evidence suggests that NAFLD is also associated with cardiovascular and chronic kidney disease [] and increased risk of hepatocellular carcinoma [–].. Sixty Wistar rats were randomly separated into experimental and control groups, which were fed with sucrose-enriched (18% simple carbohydrates) and standard diet, respectively. 518b7cbc7d