Exp Clin Endocrinol Diabetes 1999; 107(6): 343-349
DOI: 10.1055/s-0029-1212124
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Interferon-α improves glucose tolerance in diabetic and non-diabetic patients with HCV-induced liver disease

T. Konrad1 , P. Vicini2 , S. Zeuzem3 , G. Toffolo4 , D. Briem1 , J. Lormann1 , G. Herrmann5 , D. Wittmann6 , T. Lenz7 , K. Kusterer1 , G. Teuber2 , C. Cobelli4 , K.-H. Usadel1
  • 1Department of Internal Medicine I, Center of Internal Medicine, J. W. Goethe-University, Frankfurt, Germany
  • 2Center of Bioengineering, University of Washington, Seattle, USA
  • 3Department of Internal Medicine II, Center of Internal Medicine, J. W. Goethe-University, Frankfurt, Germany
  • 4Department of Electronics and Informatics, University of Padua, Italy
  • 5Institute of Pathology, J. W. Goethe-University, Frankfurt, Germany
  • 6Institute of Biological Chemistry, J. W. Goethe-University, Frankfurt, Germany
  • 7Department of Internal Medicine IV, Center of Internal Medicine, J. W. Goethe-University, Frankfurt, Germany
Further Information

Publication History

Publication Date:
14 July 2009 (online)

Summary

This pilot study was initiated to evaluate factors controlling glucose tolerance in patients with hepatitis C virus-induced liver disease before and after therapy with recombinant interferon-α (r-INF-α). Fifteen patients with histologically and serologically proven hepatitis C infection underwent oral and frequently sampled intravenous glucose tolerance tests (FSIGTT) before and after four months of therapy (6 × 106 U r-INF-α, subcutaneously, three times a week). Glucose, insulin and C-peptide data from FSIGTT were analysed using the minimal modeling technique to determine insulin sensitivity, glucose effectiveness and first and second phase insulin secretion. According to the WHO criteria 13 patients, had normal glucose tolerance; diabetes mellitus was diagnosed in 2 patients. In the morning following the last r-INF-oc injection four months later, insulin sensitivity improved significantly in hepatitis C virus-infected patients with normal glucose tolerance (2.17 ± 0.37 vs. 6.18 ± 0.94 10−4 min−1 per μU/ml, p < 0.001) and with diabetes mellitus (0.86 to 2.61; 0.46 to 1.06 10−4 min−1 per μU/ml). This effect was independent of the extent of fibrosis, virus load before treatment and therapy response. First phase insulin secretion increased in non-diabetic (139.2 ±17.1 vs. 200.0 ± 32.7, p < 0.05) and diabetic patients with HCV infection (55.24 to 118.5; 84.23 to 261.1). Moreover, free fatty acid concentrations in all HCV-infected patients were significantly reduced (0.48 ± 0.01 vs 0.21 ± 0.03 mmol/1, p < 0.01).

Therapy with recombinant interferon-α is associated with an amelioration of glucose tolerance in non-diabetic and diabetic HCV-infected patients.

Abbreviations used in this paper: ALAT, alanine-aminotransferase; ASAT, aspartate-aminotransferase; anti-TPO, thyroid peroxidase antibody; BMI, body mass index; CV, coefficient of variation; FFA, free fatty acids; FSIGTT, frequently sampled intravenous glucose tolerance test; GAD, glutamic acid decarboxylase antibody; K<3, intravenous glucose disappearance rate Φ1 O19 first phase insulin secretion; Φ2, second phase insulin secretion; SG, glucose effectiveness; SI, insulin sensitivity; STH, somatotropic hormone.

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