title: Interferon-alpha reduces insulin resistance and beta-cell secretion in responders among patients with chronic hepatitis B and C.
abstract: This study aimed at elucidating the effects of interferon (IFN)-alpha on glucose metabolism in patients with chronic hepatitis B and C infections. Twenty-eight biopsy-proven patients with chronic hepatitis B (ten cases) and hepatitis C (18 cases) were given IFN-alpha for a total of 24 weeks. The patients received a 75 g oral glucose tolerance test (OGTT), glucagon stimulation test, tests for type 1 diabetes-related autoantibodies and an insulin suppression test before and after IFN-alpha therapy. Ten of the 28 patients responded to IFN-alpha therapy. Steady-state plasma glucose of the insulin suppression test decreased significantly in responders (13.32+/-1.48 (S.E.M.) vs 11.33+/-1.19 mmol/l, P=0.0501) but not in non-responders (12.29+/-1.24 vs 11.11+/-0.99 mmol/l, P=0.2110) immediately after completion of IFN-alpha treatment. In the oral glucose tolerance test, no significant difference was observed in plasma glucose in either responders (10.17+/-0.23 vs 10.03+/-0.22 mmol/l) or non-responders (10.11+/-0.22 vs 9.97+/-0.21 mmol/l) 3 Months after completion of IFN-alpha treatment. However, significant differences were noted in C-peptide in both responders (2.90+/-0.13 vs 2.20+/-0.09 nmol/l, P=0.0040) and non-responders (2.45+/-0.11 vs 2.22+/-0.08 nmol/l, P=0.0287) before vs after treatment. The changes of C-peptide in an OGTT between responders and non-responders were also significantly different (P=0.0028), with responders reporting a greater reduction in C-peptide. No case developed autoantibodies during the treatment. In patients who were successfully treated with IFN-alpha, insulin sensitivity improved and their plasma glucose stayed at the same level without secreting as much insulin from islet beta-cells.
authors.affiliation: Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. tytai@ha.mc.ntu.edu.tw
authors.forename: T-Y
authors.initials: TY
authors.lastname: Tai
authors.forename: J-Y
authors.initials: JY
authors.lastname: Lu
authors.forename: C-L
authors.initials: CL
authors.lastname: Chen
authors.forename: M-Y
authors.initials: MY
authors.lastname: Lai
authors.forename: P-J
authors.initials: PJ
authors.lastname: Chen
authors.forename: J-H
authors.initials: JH
authors.lastname: Kao
authors.forename: C-Z
authors.initials: CZ
authors.lastname: Lee
authors.forename: H-S
authors.initials: HS
authors.lastname: Lee
authors.forename: L-M
authors.initials: LM
authors.lastname: Chuang
authors.forename: Y-M
authors.initials: YM
authors.lastname: Jeng
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000704:Analysis of Variance; D001323:Autoantibodies / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D016009:Chi-Square Distribution; D004279:DNA, Viral / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D005260:Female; D005934:Glucagon; D005951:Glucose Tolerance Test; D006513:Hepatitis B e Antigens / Q000097:blood; D019694:Hepatitis B, Chronic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D016898:Interferon-alpha; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D002096:C-Peptide; D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D007328:Insulin; D016898:Interferon-alpha; D005934:Glucagon; D000410:Alanine Transaminase