Dunn F L, Raskin P, Bilheimer D W, Grundy S M
Metabolism. 1984 Feb;33(2):117-23. doi: 10.1016/0026-0495(84)90122-7.
We examined the effect of diabetic control on very low-density lipoprotein-triglyceride (VLDL-TG) metabolism in six patients with type II (noninsulin-dependent) diabetes mellitus and marked hypertriglyceridemia. VLDL-TG transport was determined using 3H-glycerol as an endogenous precursor of VLDL-TG, and the resultant kinetic data were evaluated by multicompartmental analysis. Studies were performed in the hypertriglyceridemic diabetic subjects during poor diabetic control and again after 3 months of diabetic treatment, and the results were compared to studies in nondiabetic normolipidemic subjects and nondiabetic subjects with familial forms of hypertriglyceridemia. In the poorly controlled diabetics, mean VLDL-TG synthesis was threefold higher than in the normolipidemic subjects, and the mean fractional catabolic rate (FCR) of VLDL-TG was only one-third of the normals. With diabetic treatment, plasma triglyceride levels fell by more than 50%, but remained fourfold higher than the normals. This was associated with a decrease in mean VLDL-TG synthesis to a level similar to that observed in the genetic hyperlipidemic subjects, but still 2.6-fold higher than the normals. In addition, the mean FCR rose after diabetic control to a level slightly above that of the genetic hyperlipidemic subjects, but remained less than one-half of the normal value. However, the response of VLDL-TG kinetics to diabetic treatment was not uniform. In four subjects, control of hyperglycemia ameliorated the hypertriglyceridemia primarily by decreasing VLDL-TG overproduction. In the other two subjects, diabetic treatment had a greater effect on the FCR than an overproduction of VLDL-TG. Thus, in this select group of diabetic, hypertriglyceridemic subjects, poor diabetic control contributed to both VLDL-TG overproduction and low FCRs. Failure of diabetic treatment to restore VLDL-TG kinetic parameters to normal suggests that the hypertriglyceridemia was due not only to diabetes mellitus but also to an additional abnormality affecting lipoprotein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了糖尿病控制对6例II型(非胰岛素依赖型)糖尿病且伴有明显高甘油三酯血症患者极低密度脂蛋白甘油三酯(VLDL-TG)代谢的影响。使用3H-甘油作为VLDL-TG的内源性前体来测定VLDL-TG转运,并通过多室分析评估所得的动力学数据。在糖尿病控制不佳的高甘油三酯血症糖尿病受试者中进行研究,并在糖尿病治疗3个月后再次进行研究,且将结果与非糖尿病正常血脂受试者以及患有家族性高甘油三酯血症的非糖尿病受试者的研究结果进行比较。在控制不佳的糖尿病患者中,VLDL-TG的平均合成量比正常血脂受试者高三倍,且VLDL-TG的平均分解代谢率(FCR)仅为正常人的三分之一。经过糖尿病治疗,血浆甘油三酯水平下降超过50%,但仍比正常人高四倍。这与VLDL-TG平均合成量降至与遗传性高脂血症受试者中观察到的水平相似有关,但仍比正常人高2.6倍。此外,糖尿病控制后平均FCR升至略高于遗传性高脂血症受试者的水平,但仍不到正常值的一半。然而,VLDL-TG动力学对糖尿病治疗的反应并不一致。在4名受试者中,高血糖的控制主要通过降低VLDL-TG的过量产生来改善高甘油三酯血症。在另外两名受试者中,糖尿病治疗对FCR的影响大于VLDL-TG的过量产生。因此,在这一特定组的糖尿病、高甘油三酯血症受试者中,糖尿病控制不佳导致了VLDL-TG的过量产生和低FCR。糖尿病治疗未能将VLDL-TG动力学参数恢复正常表明,高甘油三酯血症不仅归因于糖尿病,还归因于影响脂蛋白代谢的另一种异常。(摘要截取自250字)