FOR IMMEDIATE RELEASE
October 14, 2008
Contact: Christine Guilfoy
Office: (301) 634-7253
cguilfoy@the-aps.org
Resveratrol Prevents Fat Accumulation In
Livers of ‘Alcoholic’ Mice
Study
shows substance found in grapes, red wine, peanuts, prevents alcoholic fatty
liver by coordinating molecules that control fat metabolism
BETHESDA, Md. (Oct. 14, 2008) − The
accumulation of fat in the liver as a result of chronic alcohol consumption
could be prevented by consuming resveratrol, according to a new study with
mice. The research found that resveratrol reduced the amount of fat produced
in the liver of mice fed alcohol and, at the same time, increased the rate
at which fat within the liver is broken down.
Chronic alcohol consumption causes fat to accumulate
and can lead to liver diseases, including cirrhosis and fibrosis of the
liver. It can also result in liver failure. The study points to resveratrol
as a possible treatment for alcoholic fatty liver disease, and as a way to
prevent the disease in those who are at risk, but have not developed it.
Resveratrol is present in grapes, peanuts, berries and
in red wine. Other research with mice has suggested resveratrol may have
anti-cancer and anti-inflammatory properties. There is also evidence that it
has cardiovascular benefits. However, these findings have not been extended
to humans.
The study, "Resveratrol alleviates alcoholic fatty
liver in mice," was carried out by Joanne M. Ajmo, Xiaomei Liang,
Christopher Q. Rogers, Brandi Pennock and Min You, all of the University of
South Florida Health Sciences Center, Tampa. The study appears in the
American Journal of Physiology-Gastrointestinal and Liver Physiology,
published by The American Physiological Society.
Activates cell signalers
The study builds on previous research, which suggests
that alcohol inhibits two molecules that play a role in cell signaling and
the breakdown of fats in the liver: AMP-activated protein kinase (AMPK) and
sirtuin 1 (SIRT1). When alcohol inactivates AMPK and SIRT1, it allows fat to
accumulate. Resveratrol does the opposite -- activating AMPK and SIRT1, and
helping to clear out fat.
In this study, the authors wanted to find out more
about how this happens, at the molecular level. They divided mice into
groups and fed all of them a low-fat diet. Some mice had resveratrol in
their diet, some had resveratrol plus ethanol (alcohol), some had ethanol
alone and some had neither ethanol nor resveratrol. The researchers used two
different dose levels of resveratrol. At the end of the experiment, they
examined the livers of the mice.
The researchers found, as they had expected, that
resveratrol treatment increased the expression of SIRT1 and stimulated the
activity of AMPK in the livers of mice fed alcohol. They further found that
the increased expression of SIRT1 and AMPK led to:
-
Reduction of sterol regulatory element binding protein
(SREBP-1)
-
Activation of peroxisome proliferator-activated receptor
gamma co-activator alpha (PGC-1α)
-
Elevation of circulating adiponectin, a hormone produced
by fat cells, which helps control
obesity
-
Enhanced expression of adiponectin receptors in the liver,
which increases the effectiveness of the circulating adiponectin.
The findings suggest that
resveratrol prevents alcoholic fatty liver by coordinating molecules that
control fat metabolism. This prevents accumulation of fat in the mouse liver
by both reducing the production of fat and burning off the fat that is
there. Interestingly, the combination of alcohol with resveratrol appears to
enhance the positive effects of resveratrol, said Dr. You, the study’s
senior author.
"Our study suggests that resveratrol may serve as a
promising agent for preventing or treating human alcoholic fatty liver
disease," the authors concluded.
NOTE TO EDITORS: To interview Dr. You, please
contact Christine Guilfoy at (301) 634-7253 or at
cguilfoy@the-aps.org.
Funding: National Institute on Alcoholism and
Alcohol Abuse.
***
Physiology
is the study of how molecules, cells, tissues and organs function to create
health or disease. The American Physiological Society (www.The-APS.org/press)
has been an integral part of this discovery process since it was established
in 1887.
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