果糖诱导的胰岛素抵抗大鼠模型中糖基化应激对血脂谱的损伤。

Glycoxidative stress-induced damage on lipid profile in a fructose-enriched diet model of insulin resistance in rats.

机构信息

Centro de Endocrinología Experimental y Aplicada, UNLP-CONICET La Plata, PAHO/WHO Collaborating Center, Argentina.

出版信息

Arch Physiol Biochem. 2010 Feb;116(1):42-9. doi: 10.3109/13813450903527713.

DOI:10.3109/13813450903527713

PMID:20082562

Abstract

OBJECTIVE

To study alterations in plasma lipid profile and oxidative damage to lipoprotein fractions (LF) and their fatty acids during an early insulin-resistant and increased oxidative state developed by a fructose-rich diet (FRD).

METHODS AND RESULTS

Wistar rats were fed a commercial diet with (FRD) or without (CD) 10% fructose in the drinking water. After 3 weeks, plasma glucose, triglyceride (TG), insulin (I), fructosamine (F), free fatty acids (FFA) and lipid profile (total cholesterol [TC] and HDL-C, LDL-C and VLDL-C sub-fractions) were determined. The insulin sensitivity HOMA index was assessed. FRD-fed rats had higher plasma TG, I, and F levels; increased HOMA; decreased HDL-C and LDL-C; augmented VLDL-C and TC/HDL-C, and TG/HDL-C atherogenic risk scores. LF of FRD rats had increased oxidative damage on the fatty acyl profile and in copper-induced lipoperoxidation.

CONCLUSIONS

Fructose feeding early increases the atherogenic risk inducing an insulin resistant-glycoxidative state that affects plasma lipid profiles.

摘要

目的

研究富含果糖的饮食（FRD）引起的早期胰岛素抵抗和氧化状态增加时，血浆脂质谱和脂蛋白（LF）及其脂肪酸的氧化损伤的变化。

方法和结果

Wistar 大鼠饮用含（FRD）或不含（CD）10%果糖的商业饮食。3 周后，测定血浆葡萄糖、甘油三酯（TG）、胰岛素（I）、果糖胺（F）、游离脂肪酸（FFA）和脂质谱（总胆固醇[TC]和高密度脂蛋白胆固醇[HDL-C]、低密度脂蛋白胆固醇[LDL-C]和极低密度脂蛋白胆固醇[VLDL-C]亚组分）。评估胰岛素敏感性 HOMA 指数。FRD 喂养的大鼠血浆 TG、I 和 F 水平升高；HOMA 增加；HDL-C 和 LDL-C 降低；VLDL-C 和 TC/HDL-C 增加，TG/HDL-C 动脉粥样硬化风险评分增加。FRD 大鼠的 LF 脂肪酸酰基谱和铜诱导的脂质过氧化增加了氧化损伤。