Hepatitis C virus infection enhances insulin resistance induced by visceral fat accumulation
Hepatitis C virus infection enhances insulin resistance induced by visceral fat accumulation
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DOI：
10.1111/j.1478-3231.2008.01853.x
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发表时间：
2009-02-01
影响因子：
6.7
通讯作者：
Fujimoto, Kazuma
中科院分区：
文献类型：
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作者：
Eguchi, Yuichiro;Mizuta, Toshihiko;Fujimoto, Kazuma
为了阐明内脏肥胖对丙型肝炎病毒（HCV）感染患者的影响，我们研究了胰岛素抵抗发展和内脏脂肪堆积之间的关系。我们分析了87例轻度纤维化（1期或2期）的HCV感染患者，并与125例性别和年龄匹配的非酒精性脂肪性肝病（NAFLD）患者进行了比较。通过腹部计算机断层扫描测量脐水平的内脏脂肪面积（VFA; cm（2））程度，并将其分为两个等级：无内脏肥胖，VFA < 100和内脏肥胖，VFA >= 100。采用稳态胰岛素抵抗模型（HOMA-IR）和定量胰岛素敏感性检查指数（QUICKI）评价胰岛素抵抗。通过β细胞功能的稳态模型评估（HOMA-β）评价胰腺β细胞功能。用HOMA-IR和QUICKI评估胰岛素抵抗与内脏脂肪堆积相关，HCV患者的胰岛素抵抗程度高于伴有内脏肥胖的NAFLD患者。对于每个VFA等级，HCV患者的HOMA-β均高于NAFLD患者。血清可溶性TNF受体1和2在HCV患者高于NAFLD患者内脏肥胖。丙型肝炎病毒感染是胰岛素抵抗的发展，特别是在内脏肥胖患者的危险因素。
To clarify the impact of visceral obesity on hepatitis C virus (HCV)-infected patients, we examined the relationship between insulin resistance development and visceral fat accumulation.We analyzed 87 HCV-infected patients with mild fibrosis (stage 1 or 2) in comparison with 125 sex- and age-matched patients with non-alcoholic fatty liver disease (NAFLD). The degree of visceral fat area (VFA; cm(2)) at the umbilical level was measured by abdominal computed tomography and divided into two grades: no visceral obesity, VFA < 100 and visceral obesity, VFA >= 100. Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI). Pancreatic beta-cell function was evaluated by homeostasis model assessment of beta-cell function (HOMA-beta). Serum soluble tumour necrosis factor (TNF)-receptors 1 and 2 and adiponectin were measured.Insulin resistance evaluated by HOMA-IR and QUICKI was correlated with visceral fat accumulation, and was higher in HCV patients than in NAFLD patients with visceral obesity. HOMA-beta was higher in HCV patients than in NAFLD patients for each VFA grade. Serum-soluble TNF-receptors 1 and 2 were higher in HCV patients than in NAFLD patients with visceral obesity.Hepatitis C virus infection is a risk factor for development of insulin resistance, particularly in patients with visceral obesity.