Shin Min-Jeong, Park Eunju, Lee Jong Ho, Chung Namsik
Yonsei Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Ann Nutr Metab. 2006;50(2):115-20. doi: 10.1159/000090499. Epub 2005 Dec 21.
Several studies have reported that insulin resistance and compensatory hyperinsulinemia increased lipid peroxidation, suggesting the linking to each other. We investigated the relationships between insulin resistance index HOMA-IR and lipid peroxidation, plasma antioxidant status in non-diabetic, hypercholesterolemic patients.
We measured the urinary excretion of 8-epi-prostaglandin F(2)(alpha)(PGF(2)(alpha)) levels as a measure of lipid peroxidation in vivo, total radical trapping antioxidant potential (TRAP) and fat-soluble antioxidant vitamins in 76 non-diabetic subjects with hypercholesterolemia (mean age 59 years, 25 males and 51 females). Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR) derived from fasting glucose and insulin concentrations.
HOMA-IR was positively correlated with the urinary excretion of PGF(2)(alpha) (r=0.222, p<0.05) and negatively correlated with the TRAP (r=-0.211, p<0.05) in total subjects. Furthermore, there were significant inverse relationships between HOMA-IR and lipid corrected fat-soluble vitamins such as beta-carotene (r=-0.297, p<0.01) and gamma-tocopherol (r=-0.243, p<0.05) and also significant inverse relation was found between lipid corrected beta-carotene and the urinary PGF(2)(alpha)excretion (r=-0.205, p<0.05). When total subjects were divided into three groups according to tertiles of HOMA-IR, significant differences in urinary PGF(2)(alpha)excretion (p<0.05) and lipid corrected beta-carotene (p<0.005) among the three groups were observed. The highest HOMA-IR group had the higher levels of urinary PGF(2)(alpha)excretion and lower levels of plasma beta-carotene compared with the lowest HOMA-IR group.
Our data showed that the insulin resistance of hypercholesterolemic patients increased oxidative stress and negatively influenced plasma antioxidant system. These results provide evidence in understanding mechanism linking insulin resistance and oxidative stress accompanied by reduced antioxidant system.
多项研究报告称,胰岛素抵抗和代偿性高胰岛素血症会增加脂质过氧化,提示二者之间存在关联。我们调查了非糖尿病、高胆固醇血症患者的胰岛素抵抗指数HOMA-IR与脂质过氧化、血浆抗氧化状态之间的关系。
我们测量了76名非糖尿病高胆固醇血症患者(平均年龄59岁,男性25名,女性51名)体内脂质过氧化的指标——尿8-表-前列腺素F2α(PGF2α)水平、总自由基捕获抗氧化能力(TRAP)以及脂溶性抗氧化维生素。通过空腹血糖和胰岛素浓度计算的稳态模型评估(HOMA-IR)来评估胰岛素抵抗。
在所有受试者中,HOMA-IR与PGF2α的尿排泄量呈正相关(r = 0.222,p < 0.05),与TRAP呈负相关(r = -0.211,p < 0.05)。此外,HOMA-IR与经脂质校正的脂溶性维生素如β-胡萝卜素(r = -0.297,p < 0.01)和γ-生育酚(r = -0.243,p < 0.05)之间存在显著的负相关,并且经脂质校正的β-胡萝卜素与尿PGF2α排泄量之间也存在显著的负相关(r = -0.205,p < 0.05)。当根据HOMA-IR的三分位数将所有受试者分为三组时,观察到三组之间尿PGF2α排泄量(p < 0.05)和经脂质校正的β-胡萝卜素(p < 0.005)存在显著差异。与HOMA-IR最低的组相比,HOMA-IR最高的组尿PGF2α排泄量更高,血浆β-胡萝卜素水平更低。
我们的数据表明,高胆固醇血症患者的胰岛素抵抗会增加氧化应激,并对血浆抗氧化系统产生负面影响。这些结果为理解胰岛素抵抗与伴随抗氧化系统降低的氧化应激之间的联系机制提供了证据。