✦ LIBER ✦

c-Jun NH2-terminal kinase 1 in hepatocytes: An essential mediator of insulin resistance

✍ Scribed by Francisco Javier Cubero; Oliver Drvarov; Christian Trautwein

Publisher: John Wiley and Sons
Year: 2010
Tongue: English
Weight: 365 KB
Volume: 51
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.23737

No coin nor oath required. For personal study only.

✦ Synopsis

Nonalcoholic steatosis (fatty liver) is a major cause of liver dysfunction that is associated with insulin resistance and metabolic syndrome. The cJun NH 2 -terminal kinase 1 (JNK1) signaling pathway is implicated in the pathogenesis of hepatic steatosis and drugs that target JNK1 may be useful for treatment of this disease. Indeed, mice with defects in JNK1 expression in adipose tissue are protected against hepatic steatosis. Here we report that mice with specific ablation of Jnk1 in hepatocytes exhibit glucose intolerance, insulin resistance, and hepatic steatosis. JNK1 therefore serves opposing actions in liver and adipose tissue to both promote and prevent hepatic steatosis. This finding has potential implications for the design of JNK1-selective drugs for the treatment of metabolic syndrome.

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