Maeno Tadashi, Okumura Akihiko, Ishikawa Tetsuya, Kato Koichi, Sakakibara Fumihiko, Sato Ken, Ayada Minoru, Hotta Naoki, Tagaya Tsuneaki, Fukuzawa Yoshitaka, Kakumu Shinichi
Division of Gastroenterology, Department of Internal Medicine and Research Center for Infectious Diseases, Aichi Medical University School of Medicine, Aichi, Japan.
J Gastroenterol Hepatol. 2003 Dec;18(12):1358-63. doi: 10.1046/j.1440-1746.2003.03179.x.
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.
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)-alpha 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.
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-alpha were related with HOMA-IR (BMI: r = 0.395, P = 0.041; AST: r = 0.465, P = 0.014; TNF-alpha: r = 0.396, P = 0.040). In contrast, HOMA-IR related to TNF-alpha (r = 0.526, P = 0.013) in non-diabetic patients with advanced liver fibrosis.
Collectively, hepatic fibrosis and inflammation appear to play key roles in the increase in insulin resistance in patients with chronic HCV infection.
越来越多的证据表明，慢性丙型肝炎病毒（HCV）感染患者中糖尿病（DM）的患病率更高。然而，慢性HCV感染促进糖尿病的原因尚不清楚。在本研究中，作者聚焦于非肝硬化且无糖尿病的慢性HCV感染患者，并评估了导致胰岛素抵抗增加的因素。
纳入56例诊断为HCV相关慢性肝病的患者。使用每位患者空腹过夜后采集的静脉血样本，测定包括体重指数（BMI）、天冬氨酸转氨酶（AST）、丙氨酸转氨酶、胆碱酯酶、甘油三酯、总胆固醇、血红蛋白、血小板计数、糖化血红蛋白、免疫反应性胰岛素（IRI）以及肿瘤坏死因子（TNF）-α和HCV-RNA血清水平等生化信息。还计算了胰岛素抵抗的稳态模型评估（HOMA-IR），这是一种简单便捷的胰岛素抵抗测量方法。研究了肝纤维化程度与HOMA-IR之间的关系，以及非糖尿病患者中导致HOMA-IR增加的临床因素。
胰岛素抵抗的稳态模型评估和IRI水平随纤维化进展而平行升高。在轻度至中度肝纤维化的非糖尿病患者中，BMI、AST血清水平和TNF-α与HOMA-IR相关（BMI：r = 0.395，P = 0.041；AST：r = 0.465，P = 0.014；TNF-α：r = 0.396，P = 0.040）。相比之下，在晚期肝纤维化的非糖尿病患者中，HOMA-IR与TNF-α相关（r = 0.526，P = 0.013）。
总体而言，肝纤维化和炎症似乎在慢性HCV感染患者胰岛素抵抗增加中起关键作用。
