Diabetes Care 28:940-941, 2005
© 2005 by the American Diabetes Association, Inc.
Pathophysiology/Complications Brief Report |
Hepatitis C Virus Infection and Human Pancreatic ß-Cell Dysfunction
Matilde Masini, MD1,
Daniela Campani, MD2,
Ugo Boggi, MD3,
Michele Menicagli, MD2,
Nicola Funel, MD1,
Maria Pollera, MD1,
Roberto Lupi, PHD1,
Silvia Del Guerra, PHD1,
Marco Bugliani, PHD1,
Scilla Torri, PHD1,
Stefano Del Prato, MD1,
Franco Mosca, MD3,
Franco Filipponi, MD4 and
Piero Marchetti, MD, PHD1
1 Metabolic Unit, Department of Endocrinology and Metabolism, University of Pisa and Pisa University Hospital, Pisa, Italy
2 Section of Transplantation Pathology, Division of Surgical, Molecular and Ultrastructural Pathology, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
3 Referral Center for the Treatment of Pancreas Diseases, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
4 Liver Transplant Unit, University of Pisa and Pisa University Hospital, Pisa, Italy
Address correspondence and reprint requests to Piero Marchetti, MD, Department of Endocrinology and Metabolism, Metabolic Unit, Ospedale Cisanello, Via Paradisa 2, 56124 Pisa, Italy. E-mail: marchant@immr.med.unipi.it
Abbreviations: HCV, hepatitis C virus
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INTRODUCTION
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Many patients with chronic hepatitis C virus (HCV) develop type 2 diabetes (1). This prevalence is much higher than that observed in the general population and in patients with other chronic liver diseases such as hepatitis B virus, alcoholic liver disease, and primary biliary cirrhosis. Furthermore, it has been shown that post-transplantation type 2 diabetes appears to be higher among patients with HCV (2). However, the pathogenetic basis for the association between HCV infection and diabetes has not been understood. A direct involvement of the virus in the development of insulin resistance has been proposed, and ß-cell dysfunction in HCV-positive patients has been observed in some cases (1). Because HCV can infect many tissues other than the liver (3), we hypothesized that the virus might directly damage insulin-secreting cells. This article suggests that HCV may be present in human pancreatic ß-cells and demonstrates that islet cells from HCV-positive patients have morphological and functional defects.
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RESEARCH DESIGN AND METHODS
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The pancreases of 5 HCV-positive (age 68 ± 9 years, . . . [Full Text of this Article]
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RESULTS
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CONCLUSIONS
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Copyright © 2005 by the American Diabetes Association.
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