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A common denominator of inflammations and fatty liver
Date:5/27/2008

ngly, signs of fatty liver in these animals. When Herzig specifically switched off this molecule in the liver cells of tumor-bearing mice, the lipid balance of the liver normalized within a few days. The researchers have now published their results in Hepatology.

Apart from fatty liver, highly active immune cells are another characteristic of wasting in tumor patients: Increased levels of macrophages invade fatty or liver tissue and release messaging substances such as interleukin-6 and tumor necrosis factor-alpha. The result is an inflammatory response in these organs, which eventually contributes to a disruption of metabolism and loss of energy in affected patients. Collaboration partners of Stephan Herzig in London have bred mice that completely lack the RIP140 molecule. These animals are lean and stay lean, even on a rich diet. When the researchers in Herzigs group compared these animals to normal mice, they also found that their macrophages release only small amounts of proinflammatory messaging substances. The RIP140 molecule in these inflammatory cells exercises its effect through another master regulator: the NFkB transcription factor. These results have just been published in Blood.

Thus we have put another small link into the long unknown signaling chain from tumor to tumor cachexia, says Stephan Herzig, characterizing the relevance of his two papers. Now, of course, we will search for the activator of RIP140, Herzig explains. Thus, we will proceed from one link to the next until we arrive at the tumor. And, hopefully, find the hunger signal of tumors one day.


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Contact: Dr. Stefanie Seltmann
s.seltmann@dkfz.de
Helmholtz Association of German Research Centres
Source:Eurekalert

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