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.
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.
Keywords: Diabetes mellitus, HCV, inflammatory mediators, molecular mediators, anti inflammatory.
Rights & PermissionsPrintExport