III型高脂蛋白血症患者的脂肪组织脂蛋白脂肪酶活性
Adipose tissue lipoprotein lipase activity in type III hyperlipoproteinemia.
作者信息
Goldberg A P, Applebaum-Bowden D M, Hazzard W R
出版信息
Metabolism. 1979 Nov;28(11):1122-6. doi: 10.1016/0026-0495(79)90150-1.
An impairment in the catabolism of chylomicron and very low density lipoprotein remnants appears to cause the lipid abnormalities in type III hyperlipoproteinemia. A reduction in the activity of lipoprotein lipase (LPL) has been suggested as the catabolic defect. Results in this study indicate that the activity of adipose tissue LPL measured in the fasted and fed states are in the normal range in type III hyperlipoproteinemia (fasted: type III = 2.7 +/- 1.8 mU/10(6) cells, N = 8; normals = 3.4 +/- 2.5, N = 23, p, not significant; fed: type III = 3.6 +/- 2.1, N = 7; normals = 4.8 +/- 1.8, N = 12, p, not significant). This suggests that perhaps another mechanism, such as the interaction between LPL and its lipid substrate, is abnormal, or that the activity of LPL derived from another tissue source is deficient.
乳糜微粒和极低密度脂蛋白残粒分解代谢的损害似乎导致了III型高脂蛋白血症中的脂质异常。脂蛋白脂肪酶（LPL）活性降低被认为是分解代谢缺陷。本研究结果表明，在禁食和进食状态下测量的III型高脂蛋白血症患者脂肪组织LPL活性在正常范围内（禁食：III型=2.7±1.8 mU/10(6)细胞，N = 8；正常=3.4±2.5，N = 23，p无显著性差异；进食：III型=3.6±2.1，N = 7；正常=4.8±1.8，N = 12，p无显著性差异）。这表明可能存在另一种机制异常，比如LPL与其脂质底物之间的相互作用，或者来自其他组织来源的LPL活性不足。
Zotero 插件