TONG-YUAN TAIJIN-YING LUCHI-LING CHENLai M.-Y.PEI-JER CHENJIA-HORNG KAOLee, Cha-ZeCha-ZeLeeLee, Hsuan-ShuHsuan-ShuLeeLEE-MING CHUANGYUNG-MING JENG2020-03-062020-03-0620030022-0795https://www.scopus.com/inward/record.uri?eid=2-s2.0-84983721046&doi=10.1677%2fjoe.0.1780457&partnerID=40&md5=95068072332b7726289cfcc0e8b8e684https://scholars.lib.ntu.edu.tw/handle/123456789/473493This study aimed at elucidating the effects of interferon (IFN)-α 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-α 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-α therapy. Ten of the 28 patients responded to IFN-α 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-α 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-α 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-α, insulin sensitivity improved and their plasma glucose stayed at the same level without secreting as much insulin from islet β-cells.[SDGs]SDG3alanine aminotransferase; alpha2b interferon; autoantibody; C peptide; glucagon; glucose; hemoglobin A1c; insulin; messenger RNA; octreotide; somatostatin derivative; virus DNA; adult; article; chronic hepatitis; clinical article; controlled study; drug mechanism; female; glucose blood level; glucose metabolism; hepatitis B; hepatitis C; human; human cell; human tissue; insulin dependent diabetes mellitus; insulin release; insulin resistance; insulin sensitivity; liver biopsy; male; oral glucose tolerance test; pancreas islet beta cell; priority journal; statistical analysis; steady statejournal article10.1677/joe.0.1780457129673372-s2.0-84983721046