Karakas S E, Khilnani S, Divens C, Almario R, Jen K L
Department of Medicine, Veterans' Administration Medical Center, Allen Park, MI.
Am J Clin Nutr. 1994 Feb;59(2):378-83. doi: 10.1093/ajcn/59.2.378.
We investigated the effects of the severity of the hypertriglyceridemic state on lipolysis of very-low-density lipoproteins (VLDLs) in vivo. In six patients with mild (Mild, fasting triglyceride 2.54 +/- 0.27 mmol/L) and six with moderate hypertriglyceridemia (Mod, fasting triglyceride 4.63 +/- 0.47 mmol/L), heparin infusion decreased plasma triglycerides in direct correlation with the baseline triglyceride (r = 0.92 in Mild, r = 0.96 in Mod) concentration. Fasting VLDL-triglyceride correlated inversely with postheparin lipoprotein lipase (LPL) (r = -0.85). A decrease in VLDL-triglyceride correlated with baseline VLDL-triglyceride (r = 0.93), but not with postheparin LPL. In the Mild group, low-density-lipoprotein (LDL) cholesterol steadily increased (baseline, 2.90 +/- 0.18 mmol/L; 30 min, 3.03 +/- 0.23 mmol/L; 2 h, 3.15 +/- 0.18 mmol/L) in correlation with the decrease in VLDL-triglyceride (r = 0.89). In the Mod group, LDL cholesterol initially decreased (baseline, 2.51 +/- 0.34 mmol/L; 30 min, 2.30 +/- 0.23 mmol/L) and then increased (2 h, 2.82 +/- 0.28 mmol/L). These results demonstrate a delay in conversion of VLDLs into LDLs in pronounced hypertriglyceridemia, which may contribute to the etiology of low plasma LDL cholesterol.
我们研究了高甘油三酯血症状态的严重程度对体内极低密度脂蛋白（VLDL）脂解作用的影响。在6例轻度高甘油三酯血症患者（轻度组，空腹甘油三酯2.54±0.27 mmol/L）和6例中度高甘油三酯血症患者（中度组，空腹甘油三酯4.63±0.47 mmol/L）中，静脉输注肝素后血浆甘油三酯降低，且与基线甘油三酯浓度呈直接相关（轻度组r = 0.92，中度组r = 0.96）。空腹VLDL-甘油三酯与肝素后脂蛋白脂肪酶（LPL）呈负相关（r = -0.85）。VLDL-甘油三酯的降低与基线VLDL-甘油三酯相关（r = 0.93），但与肝素后LPL无关。在轻度组中，低密度脂蛋白（LDL）胆固醇稳步升高（基线时为2.90±0.18 mmol/L；30分钟时为3.03±0.23 mmol/L；2小时时为3.15±0.18 mmol/L），与VLDL-甘油三酯的降低相关（r = 0.89）。在中度组中，LDL胆固醇最初降低（基线时为2.51±0.34 mmol/L；30分钟时为2.30±0.23 mmol/L），然后升高（2小时时为2.82±0.28 mmol/L）。这些结果表明，在明显的高甘油三酯血症中，VLDL向LDL的转化存在延迟，这可能是血浆LDL胆固醇降低病因的一个因素。
