Electronegative low density lipoprotein subform (LDL-) is increased in type 2 (non insulin dependent) microalbuminuric diabetic patients and is closely associated with LDL susceptibility to oxidation
Electronegative low density lipoprotein subform (LDL-) is increased in type 2 (non insulin dependent) microalbuminuric diabetic patients and is closely associated with LDL susceptibility to oxidation
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DOI：
10.1007/s005920050123
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发表时间：
1998-01-01
影响因子：
3.8
通讯作者：
Bon, GB
中科院分区：
文献类型：
--
作者：
Moro, E;Zambon, C;Bon, GB
越来越多的证据表明，糖尿病的特点是脂蛋白氧化增强。因此，我们研究了低密度脂蛋白氧化与微量白蛋白尿之间是否存在关系，微量白蛋白尿被认为是2型糖尿病患者血管受累的早期标志。我们选择了12例微量蛋白尿和12例正常蛋白尿2型糖尿病患者，以及12例年龄、性别和血压确定值具有可比性的对照组。用离子交换高效液相色谱法测定氧化修饰血浆LDL，简称LDL-。通过在Cu++离子存在下（滞后时间）共轭二烯形成动力学来评估LDL的体外氧化敏感性。微量蛋白尿糖尿病患者代谢控制较差，血浆甘油三酯浓度高于正常蛋白尿糖尿病患者（2.21 +/- 1.01 vs 1.15 +/- 0.39 mmol/l, P < 0.01）和对照组（1.18 +/- 0.61 mmol/l, P < 0.01）。微量蛋白尿糖尿病患者血浆LDL-百分比与正常蛋白尿糖尿病患者（5.24 +/- 1.67 vs 3.13 +/- 1.22%, P < 0.01）和对照组（2.34 +/- 1.03%,P < 0.001）相比均显著升高。与正常蛋白尿糖尿病患者（79 +/- 11 vs 97 +/- 10 min, P < 0.05）和对照组（120 +/- 24 min, P < 0.001）相比，从微量蛋白尿糖尿病患者中分离的LDL的滞后期时间显著缩短。在糖尿病患者中，LDL-百分比与果糖胺（r = 0.45, P < 0.05）、HbA(1c) （r = 0.41, P < 0.05）和甘油三酯（r = 0.65, P < 0.001）呈显著的线性相关。滞后期时间与果糖胺（r = -0.5, P < 0.01）和甘油三酯（r = -0.59, P < 0.001）呈负相关。本研究表明，微量白蛋白尿2型糖尿病患者有LDL氧化增加的证据，这似乎主要是由于代谢控制不良和更容易致动脉粥样硬化的脂质谱。
There is increasing evidence that diabetes mellitus is characterized by an enhanced lipoprotein oxidation. We have therefore investigated whether a relationship exists between LDL oxidation and microalbuminuria, which is considered an early marker of vascular involvement in type 2 diabetic patients. We selected 12 microalbuminuric and 12 normoalbuminuric type 2 diabetic patients, and 12 control subjects comparable for age, sex and blood pressure sure values. Oxidatively modified plasma LDL, referred as LDL-, were measured by ion-exchange HPLC. In vitro susceptibility to oxidation of LDL was evaluated by following the kinetics of conjugated diene formation in the presence of Cu++ ions (lag-phase time). Microalbuminuric diabetic patients had a less satisfactory metabolic control and showed a higher plasma triglyceride concentration than both normoalbuminuric diabetic patients (2.21 +/- 1.01 vs 1.15 +/- 0.39 mmol/l, P < 0.01) and controls (1.18 +/- 0.61 mmol/l, P < 0.01). The percentage of LDL- in plasma was significantly increased in microalbuminuric diabetic patients in comparison with both normoalbuminuric diabetic patients (5.24 +/- 1.67 vs 3.13 +/- 1.22%, P < 0.01) and controls (2.34 +/- 1.03%, P < 0.001). LDL isolated from microalbuminuric diabetic patients had a significantly shorter lag-phase time in comparison with normoalbuminuric diabetic patients (79 +/- 11 vs 97 +/- 10 min, P < 0.05) and controls (120 +/- 24 min, P < 0.001). In diabetic patients a significant linear correlation was observed between the percentage of LDL- and amount of fructosamine (r = 0.45, P < 0.05), HbA(1c) (r = 0.41, P < 0.05), and triglycerides (r = 0.65, P < 0.001). An inverse correlation was found between lag-phase time and fructosamine (r = -0.5, P < 0.01) and triglycerides (r = -0.59, P < 0.001). This study shows that microalbuminuric type 2 diabetic patients had evidence of increased LDL oxidation, which seems to be mainly due to a poor metabolic control and a more atherogenic lipid profile.