Premium
Hepatitis C virus infection enhances insulin resistance induced by visceral fat accumulation
Author(s) -
Eguchi Yuichiro,
Mizuta Toshihiko,
Ishibashi Eriko,
Kitajima Yoichiro,
Oza Noriko,
Nakashita Shunya,
Hara Megumi,
Iwane Shinji,
Takahashi Hirokazu,
Akiyama Takumi,
Ario Keisuke,
Kawaguchi Yasunori,
Yasutake Tsutomu,
Iwakiri Ryuichi,
Ozaki Iwata,
Hisatomi Akitaka,
Eguchi Takahisa,
Ono Naofumi,
Fujimoto Kazuma
Publication year - 2009
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2008.01853.x
Subject(s) - insulin resistance , virology , medicine , virus , hepatitis b virus , hepatitis c virus , visceral fat , insulin
Background/Aims: 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. Methods: 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 β‐cell function was evaluated by homeostasis model assessment of β‐cell function (HOMA‐β). Serum soluble tumour necrosis factor (TNF)‐receptors 1 and 2 and adiponectin were measured. Results: 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‐β 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. Conclusions: Hepatitis C virus infection is a risk factor for development of insulin resistance, particularly in patients with visceral obesity.