Molecular mediators of hepatic steatosis and liver injury.

Molecular mediators of hepatic steatosis and liver injury.
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DOI:
10.1172/jci22422
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发表时间:
2004-07
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
J. Browning;J. Horton
J. Browning;J. Horton
中科院分区:
其他
文献类型:
--
作者:
J. Browning;J. Horton

文献摘要

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肥胖及其相关的合并症是21世纪医学界面临的最普遍和最具挑战性的疾病之一。肥胖的一个主要代谢后果是胰岛素抵抗,这与肝脏中甘油三酯的沉积密切相关。肝脏脂肪变性可能是一种良性的非炎症性疾病,似乎没有不良后遗症,也可能与脂肪性肝炎有关:这种疾病可能导致终末期肝病,占美国肝脏移植的14%。在这里,我们强调了最近的进展,我们的理解的分子事件,有助于肝脂肪变性和非酒精性脂肪性肝炎。
Obesity and its associated comorbidities are among the most prevalent and challenging conditions confronting the medical profession in the 21st century. A major metabolic consequence of obesity is insulin resistance, which is strongly associated with the deposition of triglycerides in the liver. Hepatic steatosis can either be a benign, noninflammatory condition that appears to have no adverse sequelae or can be associated with steatohepatitis: a condition that can result in end-stage liver disease, accounting for up to 14% of liver transplants in the US. Here we highlight recent advances in our understanding of the molecular events contributing to hepatic steatosis and nonalcoholic steatohepatitis.