Login

Journal Image
Current Diabetes Reviews
ISSN (Print): 1573-3998
ISSN (Online): 1875-6417
VOLUME: 9
ISSUE: 6
DOI: 10.2174/15733998113096660080      Price:  $58









Underlying Pathways for Interferon Risk to Type II Diabetes Mellitus

img
Author(s): Nabil Abdel-Hamid, Taghreed Al Jubori, Amaal Farhan, Mariam Mahrous, Adel Gouri, Ezzat Awad and Johannes Breuss
Pages 472-477 (6)
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.
Affiliation:
Dean of College of Pharmacy, Kafrelsheikh University, Egypt.