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JCI online early table of contents: Feb. 16, 2009
Date:2/16/2009

a condition that may result in serious liver diseases such as hepatitis. Although the molecular events that lead to fatty liver have been determined, exactly how alcohol stimulates these has not yet been established. However, Bruce Cronstein and colleagues, at New York University School of Medicine, New York, have now established that adenosine, which is a product of the breakdown of ethanol (the alcoholic component of alcoholic beverages), has a central role in alcohol-induced fatty liver in mice. Further analysis revealed that adenosine mediated its effects in mice via two proteins, the adenosine A1 and A2B receptors. The authors therefore suggest that targeting these adenosine receptors may prove to be an effective therapy for the treatment and prevention of alcohol-induced fatty liver disease.

TITLE: Adenosine signaling contributes to ethanol-induced fatty liver in mice

AUTHOR CONTACT:
Bruce N. Cronstein
New York University School of Medicine, New York, New York, USA.
Phone: (212) 263-6404; Fax: (212) 263-1048; E-mail: cronsb01@med.nyu.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=37409


GASTROENTEROLOGY: Modulating the function of CFTR, the protein defective in cystic fibrosis

Ursula Seidler and colleagues, at Hannover Medical School, Germany, have provided new insight into the in vivo function of three proteins that interact with CFTR, the protein that is nonfunctional in individuals with cystic fibrosis, by analyzing the functional status of CFTR in the small intestine of mice lacking these proteins.

In the study, changes in CFTR-dependent secretion of HCO3 in the small intestine were analyzed in mice lacking NHERF1, NHERF2, or PDZK1. In the absence of the protein NHERF1, basal levels of secretion of HCO3 were reduced, as were levels of secretion
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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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