Excessive accumulation of fibrous
scar tissue is called fibrosis. Chronic liver diseases such as hepatitis virus
infection, nonalcoholic steatohepatitis (accumulation of fat in the liver,
along with inflammation and damage, in people who drink little or no alcohol)
and excessive alcohol consumption damage the liver tissue, cause fibrosis. Fibrosis
affects the structure and function of the liver and leads to cirrhosis, which
is a high risk factor for cancer.
The star-shaped
"stellate" cells in the liver upon activation produce collagen and
result in fibrosis. Researchers initially found high levels of vitamin D
receptor (VDR) in the stellate cell and the genome responsible for activation
of fibrosis.
"Preclinical results suggest the 'vitamin D brake' is
highly efficacious and led us to believe that the time is right to consider a
trial in the context of chronic liver disease," says Ronald M. Evans, lead
researcher and professor in Salk's Gene Expression Laboratory.
In their experiment, scientists
found that calcipotriol had a positive effect in controlling the initiation of
fibrosis in mouse liver. Authors consider this as a promising and safe strategy
in treating fibrosis. Currently there is no treatment to stop the progress of
fibrosis.
"Because there are currently
no effective drugs for liver fibrosis, we believe our findings would open a new
door for treatment," says Evans.
Researchers preferred synthetic
vitamin D to natural vitamin D due to the facts that natural vitamin D degrades
very quickly and they may increase blood calcium levels, which in turn may lead
to nausea and vomiting, frequent urination, muscle weakness, joint aches and
pain. Synthetic vitamin D, on the other hand, provides a strong response
without increasing calcium levels in the blood.
The result of the study has
encouraged the authors to plan for clinical trials for treating liver fibrosis.
The findings are published in the journal Cell.
Source: Medindia
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