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原发性高甘油三酯血症患者餐后脂肪组织脂蛋白脂肪酶活性

Postprandial adipose tissue lipoprotein lipase activity in primary hypertriglyceridemia.

作者信息

Goldberg A P, Chait A, Brunzell J D

出版信息

Metabolism. 1980 Mar;29(3):223-9. doi: 10.1016/0026-0495(80)90063-3.

Abstract

The fasting activity of adipose tissue lipoprotein lipase has been previously reported to be either normal or reduced in subjects with a primary form of hypertriglyceridemia. The postprandial activity of adipose tissue lipoprotein lipase has not been previously reported in these subjects. In subjects with primary hypertriglyceridemia the fasting lipoprotein lipase activity eluted from pieces of adipose tissue by heparin and the enzyme activity present in extracts of acetone--ether tissue powders were similar to the level of enzyme activity found in normal subjects. There also was no difference in the postprandial adipose tissue heparin-elutable lipoprotein lipase activity between these two groups when measured after high carbohydrate feeding. When the subjects with primary hypertriglyceridemia were further subdivided by genetic diagnosis, there was no difference in the level of adipose tissue lipoprotein lipase of subjects with familial hypertriglyceridemia, familial combined hyperlipidemia, or in those in whom no specific genetic diagnosis could be made. The change in lipoprotein lipase activity after feeding was inversely related to the fasting enzyme level in both the normal subjects (r = -0.58, p less than 0.05, n = 12) and the hypertriglyceridemic subjects (r = -0.92, p less than 0.01, n = 11). In the normal subjects, the plasma triglyceride response to feeding correlated inversely with the postprandial change in lipoprotein lipase activity (r = -0.76, p less than 0.02, n = 12). Adipose tissue lipoprotein lipase activity in patients with primary lipoprotein lipase deficiency was markedly reduced in the fasting state and remained essentially zero after feeding. This suggests that a functional role exists for the enzyme activity as measured.

摘要

先前有报道称,原发性高甘油三酯血症患者脂肪组织脂蛋白脂肪酶的空腹活性正常或降低。此前尚未报道过这些患者餐后脂肪组织脂蛋白脂肪酶的活性。在原发性高甘油三酯血症患者中,用肝素从脂肪组织碎片中洗脱的空腹脂蛋白脂肪酶活性以及丙酮 - 乙醚组织粉末提取物中的酶活性与正常受试者中发现的酶活性水平相似。在高碳水化合物喂养后测量时,这两组患者餐后脂肪组织肝素可洗脱脂蛋白脂肪酶活性也没有差异。当根据基因诊断对原发性高甘油三酯血症患者进一步细分时,家族性高甘油三酯血症、家族性混合性高脂血症患者或无法进行特定基因诊断的患者的脂肪组织脂蛋白脂肪酶水平没有差异。正常受试者(r = -0.58,p < 0.05,n = 12)和高甘油三酯血症患者(r = -0.92,p < 0.01,n = 11)进食后脂蛋白脂肪酶活性的变化均与空腹酶水平呈负相关。在正常受试者中,血浆甘油三酯对进食的反应与脂蛋白脂肪酶活性的餐后变化呈负相关(r = -0.76,p < 0.02,n = 12)。原发性脂蛋白脂肪酶缺乏症患者的脂肪组织脂蛋白脂肪酶活性在空腹状态下显著降低,进食后基本保持为零。这表明所测量的酶活性存在功能作用。

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