He Qing, Engelson Ellen S, Ionescu Gabriel, Glesby Marshall J, Albu Jeanine B, Kotler Donald P
Division of Gastroenterology, Department of Medicine, St. Luke's-Roosevelt Hospital Center, Columbia University, New York, NY, USA.
Antivir Ther. 2008;13(3):423-8.
A large proportion of HIV-infected patients on antiretroviral medication develop insulin resistance, especially in the context of fat redistribution. This study investigates the interrelationships among fat distribution, hepatic lipid content, and insulin resistance in HIV-infected men.
We performed a cross-sectional analysis of baseline data from 23 HIV-infected participants in three prospective clinical studies. Magnetic resonance spectroscopy was used to quantify hepatic lipid concentrations. Magnetic resonance imaging was used to quantify whole-body adipose tissue compartments: that is, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) volumes, as well as the intermuscular adipose tissue (IMAT) subcompartment and the omental-mesenteric adipose tissue (OMAT) and retroperitoneal adipose tissue (RPAT) subcompartments of VAT. The homeostasis model for assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations.
Hepatic lipid content correlated significantly with total VAT (r = 0.62, P = 0.0014), but not with SAT (r = 0.053, P = 0.81). In univariate analysis, hepatic lipid content was associated with the OMAT (r = 0.67, P = 0.0004) and RPAT (r = 0.53, P = 0.009) subcompartments; HOMA-IR correlated with both VAT and hepatic lipid contents (r = 0.61, P = 0.057 and r = 0.68, P = 0.0012, respectively). In stepwise linear regression models, hepatic lipid had the strongest associations with OMAT and with HOMA-IR.
Hepatic lipid content is associated with VAT volume, especially the OMAT subcompartment, in HIV-infected men. Hepatic lipid content is associated with insulin resistance in HIV-infected men. Hepatic lipid content might mediate the relationship between VAT and insulin resistance among treated, HIV-infected men.
很大一部分接受抗逆转录病毒药物治疗的HIV感染患者会出现胰岛素抵抗,尤其是在脂肪重新分布的情况下。本研究调查了HIV感染男性中脂肪分布、肝脏脂质含量和胰岛素抵抗之间的相互关系。
我们对三项前瞻性临床研究中23名HIV感染参与者的基线数据进行了横断面分析。磁共振波谱用于量化肝脏脂质浓度。磁共振成像用于量化全身脂肪组织区域:即皮下脂肪组织(SAT)和内脏脂肪组织(VAT)体积,以及肌肉间脂肪组织(IMAT)子区域和VAT的网膜肠系膜脂肪组织(OMAT)和腹膜后脂肪组织(RPAT)子区域。根据空腹血糖和胰岛素浓度计算胰岛素抵抗评估的稳态模型(HOMA-IR)。
肝脏脂质含量与总VAT显著相关(r = 0.62,P = 0.0014),但与SAT无关(r = 0.053,P = 0.81)。在单变量分析中,肝脏脂质含量与OMAT(r = 0.67,P = 0.0004)和RPAT(r = 0.53,P = 0.009)子区域相关;HOMA-IR与VAT和肝脏脂质含量均相关(分别为r = 0.61,P = 0.057和r = 0.68,P = 0.0012)。在逐步线性回归模型中,肝脏脂质与OMAT和HOMA-IR的关联最强。
在HIV感染男性中,肝脏脂质含量与VAT体积相关,尤其是OMAT子区域。肝脏脂质含量与HIV感染男性的胰岛素抵抗相关。肝脏脂质含量可能介导了接受治疗的HIV感染男性中VAT与胰岛素抵抗之间的关系。