Reuters Health Information (2008-03-21): Cannabinoid-blocking agents may fight alcoholic fatty liver
Cannabinoid-blocking agents may fight alcoholic fatty liver
Last Updated: 2008-03-21 8:20:06 -0400 (Reuters Health)
NEW YORK (Reuters Health) - Studies in mice provide evidence that endogenous cannabinoids are involved in the development of alcohol-induced fatty liver disease and that blocking these proteins might help fight alcoholic fatty liver disease.
Dr. George Kunos of the National Institute on Alcohol Abuse and Alcoholism and colleagues observed that chronic alcohol intake in mice led to hepatic upregulation of both CB1 cannabinoid receptors and endogenous cannabinoid 2-arachidonoylglycerol (2-AG) levels and to the development of fatty liver.
Treatment of the mice with the CB1 receptor antagonist rimonabant largely protected the animals against alcohol-induced steatosis, the team reports in the March issue of Cell Metabolism. The livers of mice fed alcohol plus rimonabant were similar in fat content as those of control mice.
Similarly, mice lacking CB1 receptors either globally or only in the liver, are resistant to alcohol-induced fatty liver disease, the team observed.
These findings "may have practical implications," Dr. Kunos said in a statement issued by Cell Press. "It suggests that the development of fatty liver in those who use alcohol could be interfered with, or perhaps reversed, with such treatment."
"Although alcoholic fatty liver is reversible in its early stages by cessation of drinking, this is often not feasible," the researchers write. "The present findings suggest that treatment with a CB1 antagonist may slow the development of steatosis and thus prevent or delay its progression to more severe and irreversible forms of liver disease."
They also note that rimonabant is being used in Europe to treat visceral obesity and the metabolic syndrome, "which themselves are known risk factors for steatosis and cirrhosis." Studies to tests the effectiveness of CB1 receptor blockers in the treatment of steatosis in humans may now be warranted, the authors conclude.
Cell Metabolism 2008;7:227-235.