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candywhy 06-19-2012 06:41 AM

Suppressor factors control the development of non-alcoholic steatohepatitis
Recently, researchers from Japan's Keio University School of Medicine, p53/p66Shc mediated signaling promotes the development of [Only registered and activated users can see links. Click Here To Register...] non-alcoholic steatohepatitis (NASH) in humans and mice. Related research published online in the Journal of Hepatology June 3. p53 is a tumor suppressor gene is a negative regulator of cell cycle and cell cycle regulation, DNA repair, cell differentiation, apoptosis, the important biological functions. p53 gene mutation (deletion) is the common events of human IL2RA tumors and tumor occurrence, development-related. Is generally believed that p53 over-expression and tumor metastasis, recurrence and poor prognosis. In this study, in order to clarify the role of p53 in non-alcoholic steatohepatitis, the researchers give the wild-type and p53-deficient male rats to a lack of methionine and choline food, eight weeks of continuous feeding induced IL2RB nutritional steatohepatitis model. They then assessed the normal liver tissue and non-alcoholic liver disease (NAFLD) in patients with mRNA expression profiles.

The study found that in the mouse NASH model in vivo,Il2rg liver cells, p53 and p66Shc signal enhancement. P53-deficient inhibition of p66Shc signal enhanced, reducing the number of intrahepatic lipid peroxidation and apoptosis in liver cells and improve the nutritional steatohepatitis. In primary cultured liver cells, transforming growth factor (TGF)-β in treatment, they found that the increase in p53 and p66Shc signal, resulting in a significant reactive oxygen IL3 species (ROS) accumulation and apoptosis. P53-deficient inhibition of TGF-β-induced p66Shc signal ROS accumulation, and liver cell apoptosis. In addition, in contrast to normal liver tissue specimens, human NAFLD liver samples of p53 and of p21 and the p66Shc the expression level was significantly improved. In patients with NAFLD, compared with simple steatosis groups, people with NASH have higher intrahepatic of p53, the level of expression of p21 and p66Shc. This indicates that there is a significant association between the expression levels of p53 and p66Sh. Overall, in liver cells, p53 control p66Shc signal level of ROS and apoptosis, regulating the progress of steatohepatitis. Moreover, these processes are likely to be involved in the regulation of TGF-β. In addition, Toshifumi Hibi, the results show that p53/p66Shc will be able to become a potential target for treatment of nonalcoholic steatohepatitis.

Zagami 02-18-2014 04:28 PM

Re: Suppressor factors control the development of non-alcoholic steatohepatitis
From Fructose-Hypertriglyceridemia to hepatic steatosis
Overconsumption of fructose, in the form of either sugar or high-fructose (cane sugar, corn syrup) in solid food or in sweetened beverages, may promote obesity and favor the development of metabolic diseases such as type 2 diabetes, dyslipidemia with increase in small dense atherogenic LDL particles, high blood pressure, albuminuria, and nonalcoholic fatty liver diseases (hepatic steatosis). In addition, hypercaloric, high-fructose diets can cause increases in a number of cardiometabolic risk factors, such as fasting and postprandial hypertriglyceridemia, ectopic lipid deposition in liver cells, impaired postprandial glucose homeostasis, and hepatic insulin resistance. Some of these effects may be related, at least in part, to the fact that fructose can be converted into fatty acids, which has been demonstrated after both acute and chronic fructose feeding. Diets high in carbohydrates, particularly sugars and even more particularly sucrose and fructose, increase serum triacylglycerol concentrations and decrease serum HDL cholesterol.
Once absorbed, dietary fructose is mainly taken up by the liver, where it is phosphorylated to fructose-1-phosphate by fructokinase and can then be converted to glycerol-3-phosphate, which serves as a backbone for triacylglycerol synthesis, VLDL production, and also decrease the catabolism of triacylglycerol-rich lipoproteins. Rates of hepatic triacylglycerol synthesis would be expected to be highest when the supply of fatty acids to the liver is also high. The likely sources of fatty acids are adipocyte lipolysis and the uptake of triacylglycerol-rich remnant particles. It is also possible that triacylglycerol stored within lipid droplets in hepatocytes can be used for VLDL synthesis. Moreover, the supply of fatty acids modulates the packaging of triacylglycerol into VLDL. The provision of fatty acids decreases apolipoprotein B degradation and therefore promotes VLDL production. The role of insulin in determining hepatic triacylglycerol and VLDL production is controversial, appearing to be acutely inhibitory but chronically stimulatory

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