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Reduced hepatic lipid content in Pten-haplodeficient mice because of enhanced AKT2/PKB beta activation in skeletal muscle

机译:由于骨骼肌中AKT2 / PKBβ活化增强,Pten单倍体缺陷小鼠肝脂质含量降低

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摘要

Background & AimsNon-alcoholic fatty liver disease (NAFLD) is a major health problem and occurs frequently in the context of metabolic syndrome and type 2 diabetes mellitus. Hepatocyte-specific Pten-deficiency in mice was shown previously to result in hepatic steatosis due to hyperactivated AKT2. However, the role of peripheral insulin-sensitive tissues on PTEN- and AKT2-dependent accumulation of hepatic lipids has not been addressed.
机译:背景与目的非酒精性脂肪肝(NAFLD)是一个主要的健康问题,在代谢综合征和2型糖尿病的背景下经常发生。先前显示小鼠肝细胞特异性Pten缺乏会由于AKT2过度活化而导致肝脂肪变性。但是,尚未解决外周胰岛素敏感组织对PTEN和AKT2依赖性肝脂质蓄积的作用。

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