Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus

ISSN: 1875-6417 (Online)
ISSN: 1573-3998 (Print)


Volume 10, 6 Issues, 2014


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Editor-in-Chief:
Norman E. Cameron
University of Aberdeen
Aberdeen, Scotland
UK


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Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus

Author(s): 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.

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.


Keywords: Diabetes mellitus, HCV, inflammatory mediators, molecular mediators, anti inflammatory.

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Article Details

Volume: 9
Issue Number: 6
First Page: 472
Last Page: 477
Page Count: 6
DOI: 10.2174/15733998113096660080
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