Hazzard E R, Bierman E L
J Lab Clin Med. 1975 Aug;86(2):239-52.
To test whether beta-migrating very low-density lipoproteins (VLDL, d less than 1.006) might not be unique to broad-beta disease (with a Type III lipoprotein pattern) but rather a caricature of an intermediate species in the catabolism of triglyceride-rich lipoproteins of normal composition and electrophoretic mobility in nonretarding media, VLDL from subjects with endogenous hypertriglyceridemia (with a Type IV pattern) or broad-beta disease were analyzed under varying dietary and pharmacologic conditions following starch-block electrophoresis. These studies revealed a spectrum in electrophoretic mobility and lipid composition throughout the Sf20 to 400 range: the more buoyant, triglyceride-rich VLDL migrated faster and the denser, triglyceride-poor VLDL more slowly, but the VLDL were broadly and continuously distributed throughout the entire beta to alpha2 regions in both disorders. However, in each subfraction of VLDL (Sf100 to 400, 60 to 100 and 20 to 60) as well as in the whole Sf20 to 400 class, the relative proportion of slower species was greater in the subjects with broad-beta disease than in those with endogenous hypertriglyceridemia. Under conditions of acutely stimulated VLDL production (following an oral fat load), a late increase in the slower species was observed as alimentary lipemia resolved. During chronic VLDL hypersecretion (with high carbohydrate feeding) both faster and slower species increased in a subject with broad-beta disease. In the same subject during clofibrate therapy, the faster species were decreased more than the slower on both normal and high carbohydrate diets. Acute acceleration of VLDL catabolism by heparin administration increased the slower VLDL at the expense of the faster, both in this subject and in a counterpart with endogenous hypertriglyceridemia. These studies are consistent with the hypothesis that slower migrating, triglyceride-poor VLDL are normal intermediate (or remnant) forms in a continuous catabolic process. The concentration of these remnants is dwarfed by that of the faster species in subjects with endogenous hypertriglyceridemia. However, in subjects with broad-beta disease they accumulate as the beta-VLDL characteristic of this disorder, most likely as a result of a relative blockade in their further catabolism.
为了检验β-迁移极低密度脂蛋白（VLDL，密度小于1.006）是否并非宽β病（Ⅲ型脂蛋白模式）所特有，而是正常组成且在非阻滞介质中具有正常电泳迁移率的富含甘油三酯脂蛋白分解代谢中间产物的一种极端形式，在淀粉阻滞电泳后的不同饮食和药理条件下，对来自内源性高甘油三酯血症（Ⅳ型模式）或宽β病患者的VLDL进行了分析。这些研究揭示了在Sf20至400范围内电泳迁移率和脂质组成的一个谱系：浮力更大、富含甘油三酯的VLDL迁移得更快，而密度更大、甘油三酯含量低的VLDL迁移得更慢，但在这两种疾病中，VLDL在整个β至α2区域广泛且连续分布。然而，在VLDL的每个亚组分（Sf100至400、60至100和20至60）以及整个Sf20至400类别中，宽β病患者中迁移较慢的组分的相对比例高于内源性高甘油三酯血症患者。在急性刺激VLDL产生的情况下（口服脂肪负荷后），随着食饵性脂血症消退，观察到迁移较慢的组分出现后期增加。在慢性VLDL分泌过多（高碳水化合物喂养）时，宽β病患者中迁移较快和较慢的组分均增加。在同一患者接受氯贝丁酯治疗期间，在正常饮食和高碳水化合物饮食中迁移较快的组分减少幅度均大于迁移较慢的组分。在该患者以及一名内源性高甘油三酯血症患者中，通过给予肝素急性加速VLDL分解代谢会以迁移较快的VLDL为代价增加迁移较慢的VLDL。这些研究与以下假设一致，即迁移较慢、甘油三酯含量低的VLDL是连续分解代谢过程中的正常中间（或残余）形式。在患有内源性高甘油三酯血症的患者中，这些残余物的浓度与迁移较快的组分相比微不足道。然而，在宽β病患者中，它们作为该疾病特有的β-VLDL积聚，很可能是由于其进一步分解代谢的相对阻滞所致。
