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.
Current Diabetes Reviews
Title:Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus
Volume: 9 Issue: 6
Author(s): Nabil Abdel-Hamid, Taghreed Al Jubori, Amaal Farhan, Mariam Mahrous, Adel Gouri, Ezzat Awad and Johannes Breuss
Affiliation:
Keywords: Diabetes mellitus, HCV, inflammatory mediators, molecular mediators, anti inflammatory.
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.
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Cite this article as:
Abdel-Hamid Nabil, Jubori Al Taghreed, Farhan Amaal, Mahrous Mariam, Gouri Adel, Awad Ezzat and Breuss Johannes, Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus, Current Diabetes Reviews 2013; 9 (6) . https://dx.doi.org/10.2174/15733998113096660080
DOI https://dx.doi.org/10.2174/15733998113096660080 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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