Hepatitis C causes insulin resistance progression to steatosis and fibrosis in genotype 1
,
Insulin
resistance is responsible for the progression to steatosis and fibrosis in
hepatitis C genotype 1, according to a French study published in the journal
Gut.
"Insulin
resistance is a common feature of chronic hepatitis C infection. But we do not
know if it could be the cause or the consequence of steatosis and
fibrosis," recalls Dr. Laetitia Fartoux, Hospital Saint- Antoine in Paris
(XII, Assistance Publique-Hôpitaux de Paris AP-HP), and colleagues.
Researchers have
attempted to elucidate this question by studying 141 patients with chronic
hepatitis C genotype 1 or 3, whereby the latter is known to cause steatosis
alone.
Participants
were not diabetic and did not have higher alcohol consumption to 20 grams per
day, two factors are also associated with the development of steatosis. They
did not suffer either from chronic cirrhosis.
Although
steatosis and fibrosis were more severe in the case of genotype 3, insulin
resistance was significantly higher in case of genotype 1 in the case of
genotype 3, associated both within steatosis. In fact, in cases of steatosis,
the median HOMA IR index was 2.1 for genotype 1 versus 1 for genotype 3.
The independent
risk factors of steatosis were insulin resistance in genotype 1 and viral load
for genotype 3. Among patients infected with HCV genotype 1, the independent
factors associated with insulin resistance were age and steatosis.
In addition, steatosis
was associated with more severe fibrosis regardless of the genotype.
For genotype 1,
although a significant relationship was observed between circulating insulin
levels and the stage of fibrosis, only steatosis and inflammatory score proved
independently correlated with fibrosis.
"This study
shows that insulin resistance appears the cause rather than the consequence of
steatosis and fibrosis in hepatitis C genotype 1 and an increase in circulating
insulin seems to be a risk factor for fibrosis through steatosis induced
insulin resistance, "the authors conclude.
Author: Mohammad
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