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The pathogenesis of nonalcoholic fatty liver disease (NAFLD) is not fully understood, and experimental models are an alternative to study this issue. 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. Sixty Wistar rats were randomly separated into experimental and control groups, which were fed with sucrose-enriched (18% simple carbohydrates) and standard diet, respectively. 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.
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. Rats that underwent physical training showed increased high-density lipoprotein- (HDL-) cholesterol levels. In conclusion, a sucrose-rich diet induced obesity, insulin resistance, oxidative stress, and NAFLD in rats. Introduction Over the last decades, obesity has become a global epidemic and an important public health problem in many countries []. This condition is largely due to excessive consumption of saturated fats and simple sugars [, ], which, associated with sedentarism, represent the modern lifestyle [].
Download Stephen King Pet Sematary Pdf Ita Free. Obesity is recognized as a risk factor for many disorders including type-2 diabetes and nonalcoholic fatty liver disease (NAFLD). NAFLD encompasses a spectrum of increasingly severe clinicopathological conditions ranging from fatty liver to steatohepatitis (NASH) with or without hepatic fibrosis/cirrhosis. Recent evidence suggests that NAFLD is also associated with cardiovascular and chronic kidney disease [] and increased risk of hepatocellular carcinoma [–]. It has been considered that insulin resistance and hyperinsulinemia play a key role in the pathogenesis of NALFD (first causative step). 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 [, ]. 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) [, ].
In spite of growing knowledge, several aspects of NAFLD pathogenesis are still unknown. Considering the difficulty in developing human studies to evaluate the influence of nutrition in the development of NAFLD and associated metabolic abnormalities, experimental models constitute a reliable alternative way.
Different animal models of NAFLD/NASH have been developed, but few of them replicate the entire human phenotype [, ]. These models may be classified into three basic categories: those caused by either spontaneous or induced genetic mutation; those produced by either dietary or pharmacological manipulation; and those involving genetic mutation and dietary or chemical challenges.
The dietary manipulations used in these last two types of models usually do not resemble human dietary pattern. In the present study, we developed a model of obesity and obesity-related NAFLD in nongenetically modified Wistar rats using a simple carbohydrate-rich diet, which resembles the current dietary pattern of humans, and followed the sequence of the pathophysiologic events and their clinical and metabolic consequences. In this context, it should be noted that, in the vast majority of studies on NAFLD in which animal models were employed, the description of the sequence of the pathophysiologic events and their consequences have not been addressed, as their key goal is usually the evaluation of a specific aspect such as a therapeutic intervention.