Goldberg A, Sherrard D J, Brunzell J D
J Clin Endocrinol Metab. 1978 Dec;47(6):1173-82. doi: 10.1210/jcem-47-6-1173.
The role of adipose tissue lipoprotein lipase (LPL) in the pathogenesis of hypertriglyceridemia in uremic patients receiving maintenance hemodialysis was evaluated. The fasting level of adipose tissue LPL activity was reduced below normal (3.4 +/- 2.5 microU/106 cells; n = 23; mean +/- SD) in hypertriglyceridemic dialysis patients (1.5 +/- 0.8; P less than 0.01; n = 15) and did not differ from normal in normotriglyceridemic dialysis patients (2.5 +/- 2.4; P = NS; n = 13). The enzyme activity increased as a function of relative body weight in normotriglyceridemic hemodialysis patients (r = 0.21; P less than 0.05) but not in the hypertriglyceridemic group (r = 0.21; P = NS). There was an abnormal response of LPL to feeding in the hypertriglyceridemic dialysis patients. The postprandial level of LPL was significantly lower in hypertriglyceridemic dialysis patients (2.2 +/- 1.0; n = 9) than in normotriglyceridemic dialysis patients (3.9 +/- 1.9; P less than 0.05; n = 10) or normal controls (4.8 +/- 1.8; P less than 0.01; n = 12). Whereas the postprandial change in LPL was inversely related to the fasting enzyme activity in normotriglyceridemic dialysis patients (r = 0.74; P less than 0.02; n = 10) and in normal controls (r = 0.58; P less than 0.05; n = 12), no such relationship existed in hypertriglyceridemic dialysis patients (r = 0.17; P = NS; n = 9). Furthermore, fasting plasma triglyceride levels in the entire group of dialysis patients were a function of the postprandial level of LPL activity (rs = 0.574; P less than 0.02; n = 19). Since the level of LPL 1) is below normal in both the fasted and fed state in the hypertriglyceridemic hemodialysis patients, 2) is normal in both the fasted and fed state in the normotriglyceridemic hemodialysis patients, and 3) in the fed state is inversely correlated with the fasting plasma triglyceride concentration in the entire group of hemodialysis patients, it is proposed that adipose tissue LPL plays a role in the etiology of hypertriglyceridemia in hemodialysis patients.
评估了脂肪组织脂蛋白脂肪酶（LPL）在接受维持性血液透析的尿毒症患者高甘油三酯血症发病机制中的作用。高甘油三酯血症透析患者（1.5±0.8；P<0.01；n = 15）的脂肪组织LPL活性空腹水平低于正常（3.4±2.5微单位/106细胞；n = 23；均值±标准差），而正常甘油三酯血症透析患者（2.5±2.4；P =无显著性差异；n = 13）的该活性与正常水平无差异。正常甘油三酯血症血液透析患者的酶活性随相对体重增加而升高（r = 0.21；P<0.05），但高甘油三酯血症组则不然（r = 0.21；P =无显著性差异）。高甘油三酯血症透析患者的LPL对进食有异常反应。高甘油三酯血症透析患者（2.2±1.0；n = 9）餐后LPL水平显著低于正常甘油三酯血症透析患者（3.9±1.9；P<0.05；n = 10）或正常对照组（4.8±1.8；P<0.01；n = 12）。正常甘油三酯血症透析患者（r = 0.74；P<0.02；n = 10）和正常对照组（r = 0.58；P<0.05；n = 12）餐后LPL变化与空腹酶活性呈负相关，而高甘油三酯血症透析患者不存在这种关系（r = 0.17；P =无显著性差异；n = 9）。此外，整个透析患者组的空腹血浆甘油三酯水平是LPL活性餐后水平的函数（rs = 0.574；P<0.02；n = 19）。鉴于1）高甘油三酯血症血液透析患者在空腹和进食状态下LPL水平均低于正常，2）正常甘油三酯血症血液透析患者在空腹和进食状态下LPL水平均正常，3）进食状态下LPL与整个血液透析患者组的空腹血浆甘油三酯浓度呈负相关，故提出脂肪组织LPL在血液透析患者高甘油三酯血症的病因中起作用。
