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Pathophysiology/Complications

Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction

  1. Matilde Masini, MD1,
  2. Daniela Campani, MD2,
  3. Ugo Boggi, MD3,
  4. Michele Menicagli, MD2,
  5. Nicola Funel, MD1,
  6. Maria Pollera, MD1,
  7. Roberto Lupi, PHD1,
  8. Silvia Del Guerra, PHD1,
  9. Marco Bugliani, PHD1,
  10. Scilla Torri, PHD1,
  11. Stefano Del Prato, MD1,
  12. Franco Mosca, MD3,
  13. Franco Filipponi, MD4 and
  14. Piero Marchetti, MD, PHD1
  1. 1Metabolic Unit, Department of Endocrinology and Metabolism, University of Pisa and Pisa University Hospital, Pisa, Italy
  2. 2Section of Transplantation Pathology, Division of Surgical, Molecular and Ultrastructural Pathology, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
  3. 3Referral Center for the Treatment of Pancreas Diseases, Department of Oncology, University of Pisa and Pisa University Hospital, Pisa, Italy
  4. 4Liver Transplant Unit, University of Pisa and Pisa University Hospital, Pisa, Italy
  1. 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
Diabetes Care 2005 Apr; 28(4): 940-941. https://doi.org/10.2337/diacare.28.4.940
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    Figure 1—

    A and B show the results obtained by an immunoperoxidase technique for anti–HCV-E2 in pancreatic islets (original magnification ×400). In A, the endocrine cells from a control pancreas are completely devoid of the viral antigen. In B, the endocrine cells from an HCV-positive pancreas show a brown, finely granular staining, indicating the presence of the HCV proteins. C and D show the results obtained by electron microscopy (original magnification ×46,000). In C, a control β-cell is shown, with the characteristic insulin granules (G) and normal mitochondria (M). In D, a β-cell from an HCV-positive pancreas is represented, showing virus-like particles (VL) close to dilated, hyperplastic Golgi apparatus (GA) and round-shaped mitochondria with dispersed matrix and fragmented cristae.

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  • Table 1—

    Insulin secretion and apoptosis data of HCV-negative and HCV-positive pancreatic islets

    Insulin release (% insulin content)
    Apoptosis
    3.3 mmol/l glucose16.7 mmol/l glucoseELISA*EM†
    HCV−1.7 ± 0.33.8 ± 0.5‡0.9 ± 0.12.0 ± 0.2
    HCV+1.6 ± 0.32.9 ± 0.4‡§1.0 ± 0.21.8 ± 0.2
    • Data are means ± SD.

    • *

      ↵* Data are expressed as arbitrary units of optical density;

    • †

      ↵† data are expressed as percentage of apoptotic β-cell over total number of counted β-cells;

    • ‡

      ↵‡ P < 0.01 vs. 3.3 mmol/l and

    • §

      ↵§ P < 0.05 vs. 16.7 mmol/l glucose, HCV− by the two-tailed Student’s t test. ELISA, enzyme-linked immunosorbent assay; EM, electron microscopy.

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Diabetes Care: 28 (4)

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April 2005, 28(4)
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Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction
Matilde Masini, Daniela Campani, Ugo Boggi, Michele Menicagli, Nicola Funel, Maria Pollera, Roberto Lupi, Silvia Del Guerra, Marco Bugliani, Scilla Torri, Stefano Del Prato, Franco Mosca, Franco Filipponi, Piero Marchetti
Diabetes Care Apr 2005, 28 (4) 940-941; DOI: 10.2337/diacare.28.4.940

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Hepatitis C Virus Infection and Human Pancreatic β-Cell Dysfunction
Matilde Masini, Daniela Campani, Ugo Boggi, Michele Menicagli, Nicola Funel, Maria Pollera, Roberto Lupi, Silvia Del Guerra, Marco Bugliani, Scilla Torri, Stefano Del Prato, Franco Mosca, Franco Filipponi, Piero Marchetti
Diabetes Care Apr 2005, 28 (4) 940-941; DOI: 10.2337/diacare.28.4.940
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