Hepatitis C Virus Infection and Human Pancreatic β-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
- 1Metabolic Unit, Department of Endocrinology and Metabolism, University of Pisa and Pisa University Hospital, Pisa, Italy
- 2Section of Transplantation Pathology, Division of Surgical, Molecular and Ultrastructural Pathology, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
- 3Referral Center for the Treatment of Pancreas Diseases, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
- 4Liver 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{at}immr.med.unipi.it
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 β-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 β-cells and demonstrates that islet cells from HCV-positive patients have morphological and functional defects.
RESEARCH DESIGN AND METHODS
The pancreases of 5 HCV-positive (age 68 ± 9 years, 3 …
