The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes
The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes
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DOI：
10.1016/s0021-9150(00)00499-8
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发表时间：
2001-02-01
期刊：
影响因子：
5.3
通讯作者：
Frenneaux, MP
中科院分区：
文献类型：
--
作者：
Anderson, RA;Evans, ML;Frenneaux, MP
餐后脂血症（PPL）是动脉粥样硬化形成的一个因素，并导致健康个体可逆的内皮功能障碍。氧化应激和富含甘油三酯（TG）的脂蛋白有牵连。本文对12例2型糖尿病（NIDDM）和12例正常对照者的PPL、内皮功能障碍（EF）和氧化应激反应进行了研究。受试者进行了脂肪耐量试验，通过血流介导的血管舒张和氧化应激来评估内皮功能，通过离体静脉脂质衍生的自由基和餐后阶段的脂质过氧化产物来测量。空腹TG、餐后高甘油三酯血症和所有脂蛋白的TG富集在NIDDM中显著更大。餐后内皮功能与空腹HDL-C呈负相关（r =-0.84，P =0.0001）。NIDDM组EF的恶化也与VLDL和LDL的TG富集相关。两组中的PPL也导致氧化应激增加。在两组中，自由基的增加与VLDL的TG富集相关，因此，在NIDDM中更大。因此，PPL-与VLDL的TG富集的产生-在两组中通过氧化应激机制导致内皮功能障碍。在NIDDM中的幅度更大。空腹HDL-C似乎有助于保护内皮细胞免受这种现象的影响。因此，与HDL-C降低相关的过度PPL可能在血管疾病的发病机制中很重要，特别是在NIDDM中。(C)2001爱思唯尔科学爱尔兰有限公司保留所有权利。
Post-prandial lipaemia (PPL) is a factor in atherogenesis and results in reversible endothelial dysfunction in healthy individuals. Oxidative stress and triglyceride (TG)-rich lipoproteins have been implicated. Type 2 diabetes (NIDDM) results in exaggerated PPL. We attempted to delineate the mechanisms of PPL induced, endothelial dysfunction (EF) and oxidative stress in 12 NIDDM and 12 matched healthy subjects. Subjects underwent a fat tolerance test, with endothelial function assessed by flow-mediated vasodilatation and oxidative stress measured by venous lipid-derived free radicals ex vivo and lipid peroxidation products over the postprandial phase. Fasting TG, post-prandial hypertriglyceridaemia and the TG enrichment of all lipoproteins was significantly greater in NIDDM. Post-prandial endothelial function inversely correlated with fasting HDL-C (r = - 0.84, P = 0.0001 in both the control and NIDDM groups. The deterioration in EF in the NIDDM group also correlated with TG enrichment of VLDL and LDL. PPL in both groups also resulted in increased oxidative stress. The increment in free radicals correlated with TG enrichment of VLDL in both groups and was, therefore, greater in NIDDM, Thus, PPL - with the production of TG-enrichment of VLDL - results in endothelial dysfunction by an oxidative stress mechanism in both groups. The magnitude is greater in NIDDM. Fasting HDL-C appears to contribute to the protection of the endothelium against this phenomenon. Hence, exaggerated PPL associated with reduced HDL-C may be important in the pathogenesis of vascular disease, particularly in NIDDM. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.