@article {Abdel-Hamid:2013:1573-3998:472,
title = "Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus",
journal = "Current Diabetes Reviews",
parent_itemid = "infobike://ben/cdr",
publishercode ="ben",
year = "2013",
volume = "9",
number = "6",
publication date ="2013-11-01T00:00:00",
pages = "472-477",
itemtype = "ARTICLE",
issn = "1573-3998",
url = "https://www.ingentaconnect.com/content/ben/cdr/2013/00000009/00000006/art00005",
keyword = "inflammatory mediators, HCV, molecular mediators, Diabetes mellitus, anti inflammatory",
author = "Abdel-Hamid, Nabil and Al Jubori, Taghreed and Farhan, Amaal and Mahrous, Mariam and Gouri, Adel and Awad, Ezzat and Breuss, Johannes",
abstract = "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.",
}