Reaven P D, Herold D A, Barnett J, Edelman S
Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla 92093-0682, USA.
Diabetes Care. 1995 Jun;18(6):807-16. doi: 10.2337/diacare.18.6.807.
To evaluate the effect of vitamin E supplementation on the susceptibility of low-density lipoprotein (LDL) and LDL subfractions to oxidation and on protein glycation in non-insulin-dependent diabetes mellitus (NIDDM).
Twenty-one men with NIDDM (HbA1c = 6-10%), ages 50-70, were randomly assigned to either 1,600 IU/day of vitamin E or placebo for 10 weeks after a 4-week placebo period. LDL and LDL subfractions were isolated after 4 weeks of placebo and after 6 and 10 weeks of therapy. Susceptibility of LDL to copper-mediated oxidation was measured by conjugated diene formation (lag time) and formation of thiobarbituric acid-reactive substances (TBARS). Fasting serum glucose, mean weekly blood glucose, HbA1c, and glycated plasma protein concentrations were also determined at these time points.
Vitamin E content in plasma and LDL increased 4.0- and 3.7-fold, respectively, in the vitamin E-treated group. Vitamin E decreased the susceptibility of LDL to oxidation in comparison with placebo (lag time, 243 +/- 46 vs. 151 +/- 22 min, P < 0.01; 3 h TBARS, 24 +/- 12 vs. 66 +/- 18 nmol malondialdehyde/mg LDL, P < 0.05). Vitamin E content also increased significantly in both buoyant and dense LDL subfractions, and their oxidation was dramatically reduced. The lag time of LDL oxidation correlated well with the content of vitamin E in both LDL and its subfractions (r = 0.69-0.92). Glycemic indexes did not change significantly in either group during the study. Protein glycation, including glycated hemoglobin, glycated albumin, glycated total plasma proteins, and glycated LDL were unchanged in the vitamin E group.
Supplementation of vitamin E in NIDDM leads to enrichment of LDL and LDL subfractions and reduced susceptibility to oxidation. Despite a greater percentage increase in vitamin E content in small dense LDL, it remained substantially more susceptible to oxidation than was buoyant LDL. This suggests that dense, LDL may gain less protection against oxidation from antioxidant supplementation than does larger, more buoyant LDL. In contrast to previous reports, vitamin E supplementation did not reduce glycation of intracellular or plasma proteins.
评估补充维生素E对非胰岛素依赖型糖尿病（NIDDM）患者低密度脂蛋白（LDL）及其亚组分氧化易感性以及蛋白质糖基化的影响。
21名年龄在50 - 70岁之间的NIDDM男性患者（糖化血红蛋白HbA1c = 6 - 10%），在经过4周的安慰剂期后，被随机分为两组，一组每天服用1600 IU维生素E，另一组服用安慰剂，为期10周。在安慰剂期4周后以及治疗6周和10周后分离LDL及其亚组分。通过共轭二烯形成（延迟时间）和硫代巴比妥酸反应性物质（TBARS）的形成来测量LDL对铜介导氧化的易感性。在这些时间点还测定空腹血糖、平均每周血糖、HbA1c以及糖化血浆蛋白浓度。
维生素E治疗组血浆和LDL中的维生素E含量分别增加了4.0倍和3.7倍。与安慰剂相比，维生素E降低了LDL的氧化易感性（延迟时间，243±46分钟对151±22分钟，P < 0.01；3小时TBARS，24±12对66±18 nmol丙二醛/毫克LDL，P < 0.05）。在漂浮型和致密型LDL亚组分中维生素E含量也显著增加，并且它们的氧化显著减少。LDL氧化的延迟时间与LDL及其亚组分中维生素E的含量密切相关（r = 0.69 - 0.92）。在研究期间两组的血糖指标均无显著变化。维生素E组中包括糖化血红蛋白、糖化白蛋白、糖化总血浆蛋白和糖化LDL在内的蛋白质糖基化没有改变。
在NIDDM患者中补充维生素E会导致LDL及其亚组分中维生素E富集，并降低氧化易感性。尽管小而致密的LDL中维生素E含量的增加百分比更大，但它仍然比漂浮型LDL更容易被氧化。这表明致密型LDL从抗氧化剂补充中获得的抗氧化保护可能比大的、更漂浮的LDL少。与先前的报道相反，补充维生素E并没有减少细胞内或血浆蛋白的糖基化。
