Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus
Nabil Abdel-Hamid, Taghreed Al Jubori, Amaal Farhan, Mariam Mahrous, Adel Gouri, Ezzat Awad and Johannes Breuss
Affiliation: Dean of College of Pharmacy, Kafrelsheikh University, Egypt.
Keywords: Diabetes mellitus, HCV, inflammatory mediators, molecular mediators, anti inflammatory.
It has been known that chronic liver treatments interfere with blood glucose metabolism. It was recognized that
diabetes mellitus among chronic hepatitis C was greater in other types of chronic liver diseases. Hepatitis C directly promotes
insulin resistance through the proteosomal degradation of insulin resistance substrate. It suppressed hepatocyte glucose
uptake through down-regulation of surface expression of glucose transporter. Long-term exposure to cytokine over
expression seems to be cytotoxic to both beta cells of the pancreas and to hepatocytes. Elevated tumor necrosis factor-a,
or its neutralization, increased insulin sensitivity. Interferon-a may also elevate the serum level of interleukin-1 which is
cytotoxic to pancreatic islet cells. Both Diabetes mellitus and resistance to interferon-a therapy are abnormally mediated
by over-expression of suppressor of cytokine signaling-1 in hepatocytes of chronic hepatitis C patients.
Conclusion: These data suggest that interferon-a therapy should be administered with caution in patients showing any
predisposition to Diabetes mellitus. Anti inflammatory therapy is critically recommended as a protector against disease
development due to cytokine mediated Diabetes mellitus during hepatitis C therapy, since inflammation seems to be a
main candidate to interferon suspected diabetogenesis.
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