Moro E, Zambon C, Pianetti S, Cazzolato G, Pais M, Bittolo Bon G
Second Department of Internal Medicine and Metabolic Diseases, Regional General Hospital, Venice, Italy.
Acta Diabetol. 1998 Oct;35(3):161-4. doi: 10.1007/s005920050123.
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 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 (2.211+/-1.01 vs 1.15+/-0.39 mmol/l, P<0.O1) 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), HbA1c (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.
越来越多的证据表明,糖尿病的特征是脂蛋白氧化增强。因此,我们研究了低密度脂蛋白(LDL)氧化与微量白蛋白尿之间是否存在关联,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物。我们选取了12例微量白蛋白尿的2型糖尿病患者、12例正常白蛋白尿的2型糖尿病患者以及12例年龄、性别和血压值相匹配的对照者。通过离子交换高效液相色谱法测定氧化修饰的血浆LDL(称为LDL-)。通过跟踪在铜离子存在下共轭二烯形成的动力学(滞后期时间)来评估LDL体外氧化的敏感性。微量白蛋白尿的糖尿病患者代谢控制较差,血浆甘油三酯浓度高于正常白蛋白尿的糖尿病患者(2.211±1.01 vs 1.15±0.39 mmol/L,P<0.01)和对照者(1.18±0.61 mmol/L,P<0.01)。与正常白蛋白尿的糖尿病患者(5.24±1.67 vs 3.13±1.22%,P<0.01)和对照者(2.34±1.03%,P<0.001)相比,微量白蛋白尿的糖尿病患者血浆中LDL-的百分比显著升高。与正常白蛋白尿的糖尿病患者(79±11 vs 97±10分钟,P<0.05)和对照者(120±24分钟,P<0.001)相比,从微量白蛋白尿的糖尿病患者分离出的LDL滞后期时间明显更短。在糖尿病患者中,观察到LDL百分比与果糖胺量(r=0.45,P<0.05)、糖化血红蛋白(HbA1c)(r=0.41,P<0.05)和甘油三酯(r=0.65,P<0.001)之间存在显著的线性相关性。发现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)之间呈负相关。这项研究表明,微量白蛋白尿的2型糖尿病患者存在LDL氧化增加的证据,这似乎主要归因于代谢控制不佳和更易致动脉粥样硬化的血脂谱。