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hepatolenticular degeneration/triglyceride
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Alterations of lipid metabolism in Wilson disease.
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BACKGROUND
Wilson disease (WD) is an inherited disorder of human copper metabolism, characterised by accumulation of copper predominantly in the liver and brain, leading to severe hepatic and neurological disease. Interesting findings in animal models of WD (Atp7b-/- and LEC rats) showed altered
Nonalcoholic fatty liver disease in asymptomatic Brazilian adolescents.
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OBJECTIVE
To evaluate the prevalence and clinical characteristics of Nonalcoholic fatty liver disease (NAFLD) among asymptomatic Brazilian adolescents.
METHODS
Transversal observational study included asymptomatic adolescents with central obesity from private and public schools in Salvador-Bahia,
Correlations between anthropometric and serologic elements of metabolic syndrome and histopathologic features of nonalcoholic fatty liver disease.
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OBJECTIVE
Studying the correlation between elements of metabolic syndrome and histological changes of the liver in nonalcoholic fatty liver disease.
METHODS
Thirty-nine patients with nonalcoholic fatty liver disease were included in our study. Inclusion criteria were: presence of liver steatosis on
ATP7B knockout disturbs copper and lipid metabolism in Caco-2 cells.
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Intestinal cells control delivery of lipids to the body by adsorption, storage and secretion. Copper (Cu) is an important trace element and has been shown to modulate lipid metabolism. Mutation of the liver Cu exporter ATP7B is the cause of Wilson disease and is associated with Cu accumulation in
The Function of ATPase Copper Transporter ATP7B in Intestine.
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Wilson disease is a disorder of copper (Cu) misbalance caused by mutations in ATP7B. ATP7B is highly expressed in the liver-the major site of Cu accumulation in patients with Wilson disease. The intestine also expresses ATP7B, but little is known about the contribution of intestinal ATP7B to normal
Targeted inactivation of copper transporter Atp7b in hepatocytes causes liver steatosis and obesity in mice.
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Copper-transporting ATPase 2 (ATP7B) is essential for mammalian copper homeostasis. Mutations in ATP7B result in copper accumulation, especially in the liver, and cause Wilson disease (WD). The major role of hepatocytes in WD pathology is firmly established. It is less certain whether the excess Cu
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