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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.

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Author: Mohammad
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