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Postheparin plasma triglyceride lipases in chronic hemodialysis: evidence for a role for hepatic lipase in lipoprotein metabolism.
Authors:D Applebaum-Bowden  A P Goldberg  W R Hazzard  D J Sherrard  J D Brunzell  J K Huttunen  E A Nikkila  C Ehnholm
Affiliation:1. Northwest Lipid Research Clinic, Department of Medicine, School of Medicine, University of Washington, Seattle, Washington USA;2. the Department of Medicine, Kuopio Medical School, Kuopio, Finland;3. the Third Department of Medicine, University of Helsinki, Finland.
Abstract:
Elevated plasma triglyceride levels frequently occur in patients with chronic renal failure receiving longterm hemodialysis. Postheparin plasma lipolytic activity, an indirect measure of triglyceride removal, is low in hemodialysis patients, but this activity measures both hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL). To determine if HTGL and/or LPL are low in hemodialysis patients and related to lipoprotein lipid levels, both activities were measured by a selective antibody-inhibition technique in postheparin plasma from 20 hemodialysis patients with a wide range of plasma triglyceride levels (104–676 mg100 ml), and the relationships between the enzyme activities and lipoprotein lipid levels were examined. To more accurately compare subjects, the heparin doses were adjusted for the differences in plasma volumes between the hemodialysis patients and the nonuremic control subjects. Hemodialysis patients with elevated plasma triglyceride levels (↑TG) had HTGL levels (148 ± 67 nmole/min/ml, n=10) which were similar to the dialysis patients with normal triglyceride levels (nlTG) (134 ± 64 nmole/min/ml, n=10) and both groups were significantly lower (p<0.05, p<0.02, respectively) than the levels of the control subjects (208 ± 61 nmole/min/ml, n=11). The HTGL levels of the hemodialysis patients with ↑TG correlated inversely with plasma total cholesterol (rs=−0.833, p<0.01) and the d>1.006 fraction cholesterol (low + high density lipoproteins, rs=−0.863,p<0.01), but not triglyceride. The activity of HTGL of the entire group of hemodialysis patients correlated with the plasma total cholesterol (rs=−0.615, p<0.01), d>1.006 fraction cholesterol (rs=−0.731, p<0.01) and low density lipoprotein cholesterol (rs=−0.659, p<0.01). The LPL levels of the hemodialysis patients with the ↑TG (52 ± 24 nmole/min/ml) were lower than those with nlTG (70 ± 25 nmole/min/ml) and the levels of both hemodialysis groups were significantly lower (p<0.01, p<0.02, respectively) than the LPL levels in the control subjects (110 ± 43 nmole/min/ml). The ratio of LPL to total postheparin plasma lipolytic activity was lower in the hemodialysis patients with ↑TG (0.32 ± 0.15), than in the hemodialysis patients with nlTG (0.47 ± 0.18, p<0.06) or the control subjects (0.45 ± 0.09, p<0.05). Unlike HTGL, the levels of LPL did not correlate with lipid levels in the hemodialysis patients. Thus, both postheparin plasma HTGL and LPL are low in hemodialysis patients. The relationship between HTGL and low density lipoprotein cholesterol levels suggests a possible role for HTGL in low density lipoprotein catabolism.
Keywords:Address reprint requests to Deborah Applebaum-Bowden   Ph.D.   Northwest Lipid Research Clinic   326 Ninth Avenue   Seattle   Wash. 98104.
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