
Fatty liver disease is becoming
increasingly common in many parts of the world, affecting about 25% of people
globallyÂ
It
is linked to obesity, type 2 diabetes and other disorders characterized by
insulin resistance.Â
Fatty Liver and its Treatment
Fatty liver
occurs when too much fat builds up in liver cells. Although it is normal
to have a tiny amount of fat in these cells, the liver is considered fatty if
more than 5% of it is fat
While
drinking too much alcohol can lead to fatty liver, in many cases it
does not play a role.
A number of
fatty liver conditions fall under the broad category of non-alcoholic liver
disease (NAFLD), which is the most common liver disease in adults and children
in Western countriesÂ
READ ABOUT:Â Hepatitis B in details
Non-alcoholic fatty liver disease (NAFLD) is an accumulation of excess
fat in the liver of people who consume little or no alcohol. It is a common
condition in obese individuals or people with diabetes. There is currently no
medication available to treat the condition
In the study, the researchers examined what happens on a cellular and molecular
level in mouse and human livers overloaded with fat, and what may be done to
help restore the damage. They found that liver macrophages, a type of white
blood cells important for the immune system, respond to the unwanted fat by
trying to burn it. In the process, these immune cells end up producing
excessive amounts of oxidants that cause damage to the liver. Further
investigation revealed that an antioxidant protein called NRF2, which usually
protects the body from harmful oxidants, was completely shut down in the liver
of the obese patients and mice.
READ ABOUT:Â Blood Urea Nitrogen (BUN)
This lack of NRF2 protein tells us that obese individuals do not have
the ability to properly respond to oxidative stress induced by fat accumulation
in the liver," says Valerio Azzimato, a researcher at the Department of
Medicine in Huddinge, Karolinska Institutet.
The researchers also found elevated levels of a small non-coding RNA molecule,
or a microRNA, called miR144 in the livers of obese individuals and mice. Both
the immune cells and the liver's most abundant cells, the hepatocytes, produce
more of this specific microRNA in response to oxidative stress. The miR144
molecule affects the NRF2 gene by decreasing its protein levels, which leads to
a weaker antioxidant response, according to the researchers.
Using a technology that enables the silencing of specific genes in liver
macrophages, the researchers were able to suppress the expression of miR144 in
the immune cells. This lowered the amounts of oxidants produced in the whole
liver and restored the antioxidant response, suggesting crosstalk between the
macrophage and hepatocyte liver cells.
Given that using exogenous antioxidants has been associated with
long-term side effects in several tissues, researchers believe that targeting
miR144 to increase the endogenous antioxidant response represents a promising
therapeutic strategy for the treatment of liver diseases in obese patients
including non-alcoholic steatohepatitis which is becoming a major cause of
liver cancer worldwide and currently has no pharmacological treatment.
No comments:
Post a Comment
Due to the high number of spammy comments we have decided to initiate comment moderation so that we can maintain our quality standards and make good environment for our visitors. Please leave your comment