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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

Japan, have established that persistent activation of the protein PPAR-alpha is required for the development of HCC in mice engineered to express the HCV core protein (HCVcpTg mice).

HCVcpTg mice develop HCC that is preceded by a condition known as either fatty liver or hepatic steatosis, which is the accumulation of fat in liver cells. In the study, HCVcpTg mice expressing two functional copies of the Ppara gene developed severe hepatic steatosis followed by HCC. However, neither HCVcpTg mice expressing one functional copy of the Ppara gene nor HCVcpTg mice lacking both functional copies of the Ppara gene developed hepatic steatosis and HCC. Consistent with the idea that sustained activation of PPAR-alpha is required for hepatic steatosis and HCC, treatment of HCVcpTg mice expressing one functional copy of the Ppara gene with a PPAR-alpha agonist induced hepatic steatosis and HCC. These data have important clinical implications and led the authors to suggest that they might provide new avenues for the development of therapeutic and nutritional approaches to the treatment of individuals chronically infected with HCV.

TITLE: PPAR-alpha activation is essential for HCV core proteininduced hepatic steatosis and hepatocellular carcinoma in mice

AUTHOR CONTACT:
Naoki Tanaka
Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan.
Phone: Phone: 81-263-37-2850; Fax: 81-263-37-3094; E-mail: naopi@hsp.md.shinshu-u.ac.jp.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33594


PULMONARY: Understanding how carbon dioxide can impair lung function

Increased levels of carbon dioxide (CO2) in the blood are detected in individuals with several lung diseases, including chronic obstructive pulmonary disease (COPD) and asthma. In individuals with COPD, raised
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