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Mechanisms of increased insulin resistance in non‐cirrhotic patients with chronic hepatitis C virus infection
Author(s) -
MAENO TADASHI,
OKUMURA AKIHIKO,
ISHIKAWA TETSUYA,
KATO KOICHI,
SAKAKIBARA FUMIHIKO,
SATO KEN,
AYADA MINORU,
HOTTA NAOKI,
TAGAYA TSUNEAKI,
FUKUZAWA YOSHITAKA,
KAKUMU SHINICHI
Publication year - 2003
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2003.03179.x
Subject(s) - medicine , insulin resistance , diabetes mellitus , gastroenterology , endocrinology , insulin , triglyceride , body mass index , alanine transaminase , cholesterol
Background and Aim: Evidence showing a higher prevalence of diabetes mellitus (DM) in patients with chronic hepatitis C virus (HCV) infection has been accumulating. However, the reason why chronic HCV infection promotes DM remains unknown. In the present study, the authors focused on non‐cirrhotic and non‐diabetic patients with chronic HCV infection and evaluated the factors responsible for increases in insulin resistance. Methods: Fifty‐six patients diagnosed with HCV‐related chronic liver disease were included. Biochemical information including body mass index (BMI), aspartate aminotransferase (AST), alanine aminotransferase, cholinesterase, triglyceride, total cholesterol, hemoglobin, platelet count, glycosylated hemoglobin, immunoreactive insulin (IRI), and serum levels of tumor necrosis factor (TNF)‐α and HCV‐RNA were determined using venous blood samples obtained from each patient after overnight fasting. Homeostasis model assessment of insulin resistance (HOMA‐IR), a simple and convenient measure of insulin resistance, was also calculated. The relationship between the stage of liver fibrosis and HOMA‐IR, and the clinical factors responsible for the increase in HOMA‐IR in non‐diabetic patients was investigated. Results: Homeostasis model assessment of insulin resistance and IRI levels increased parallel with the progression of fibrosis. Among the non‐diabetic patients with mild to moderate liver fibrosis, BMI, serum levels of AST and TNF‐α were related with HOMA‐IR (BMI: r = 0.395, P = 0.041; AST: r = 0.465, P = 0.014; TNF‐α: r = 0.396, P = 0.040). In contrast, HOMA‐IR related to TNF‐α ( r = 0.526, P = 0.013) in non‐diabetic patients with advanced liver fibrosis. Conclusion: Collectively, hepatic fibrosis and inflammation appear to play key roles in the increase in insulin resistance in patients with chronic HCV infection.