Hepatic Triglyceride Lipase Activity Research Articles

Serum lipids and postheparin plasma lipase activity in Japanese children with ketosis-prone diabetes mellitus.

Using a selective immunochemical method, the activities of postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) were measured in 7 children with newly diagnosed IDDM, 39 on a conventional subcutaneous insulin regimen (CSC), and 11 children receiving continuous subcutaneous infusion of insulin (CSII). The newly diagnosed untreated patients frequently had hypertriglyceridemia and a decreased serum HDL-cholesterol level, while they showed a mild, but not significant increase of the serum total cholesterol level. The insulin-treated patients (both on CSC and on CSII) had serum lipid levels similar to those in controls. LPL activity was decreased in untreated patients, and insulin treatment resulted in an increase in the LPL activity with a concomitant normalization of serum triglyceride and HDL-cholesterol levels. In contrast to the patients on CSII who had normal LPL activity, patients on CSC had an increased LPL activity. This may have been due to peripheral hyperinsulinemia. HTGL activity did not show any increase during the time of improved diabetic control. In conclusion; (1) serum lipid levels were normal both in the patients on CSC and CSII. (2) LPL activity was normal on CSII, but was increased on CSC and decreased in untreated patients.

先天性レシチン: コレステロールアシルトランスフェラーゼ欠損症に対する食事療法の効果

To study the disturbance of metabolism of plasma lipids and apoproteins in a familial lecithin: cholesterol acyltransferase deficiency, the effects of a low fat diet on plasma lipids, apoproteins and plasma enzyme activities were investigated. The plasma apoprotein A-1 and E levels were measured by a radioimmunoassay. The apoprotein B level was determined by the method of a single radial immunodiffusion. Lipoprotein lipase and hepatic triglyceride lipase activities were measured by an immunochemical method utilizing antiserum prepared against hepatic triglyceride lipase. By the restriction of fat in diet, the amount of triglyceriderich lipoproteins were decreased. Also, plasma apoprotein E and B levels were markedly decreased, while the improvements of both lipoprotein lipase and hepatic triglyceride lipase was not observed. These results suggest that high plasma apoprotein E in the familial lecithin: cholesterol acyltransferase deficiency is strongly related to the disturbed triglyceride-rich lipoprotein metabolism in the lecithin: cholesterol acyltransferase deficient state.

Lipoprotein metabolism during acute inhibition of hepatic triglyceride lipase in the cynomolgus monkey.

The role of the enzyme hepatic triglyceride lipase was investigated in a primate model, the cynomolgus monkey. Antisera produced against human postheparin hepatic lipase fully inhibited cynomolgus monkey posttheparin plasma hepatic triglyceride lipase activity. Lipoprotein lipase activity was not inhibited by this antisera. Hepatic triglyceride lipase activity in liver biopsies was decreased by 65-90% after intravenous infusion of this antisera into the cynomolgus monkey. After a 3-h infusion of the antisera, analytic ultracentrifugation revealed an increase in mass of very low density lipoproteins (S(f) 20-400). Very low density lipoprotein triglyceride isolated by isopycnic ultracentrifugation increased by 60-300%. Analytic ultracentrifugation revealed an increase in mass of lipoproteins with flotation greater than S(f) 9 (n = 4). The total mass of intermediate density lipoproteins (S(f) 12-20) approximately doubled during the 3 h of in vivo enzyme inhibition. While more rapidly floating low density lipoproteins (S(f) 9-12) increased, the total mass of low density lipoproteins decreased after infusion of the antibodies. The changes in high density lipoproteins did not differ from those in control experiments. In order to determine whether the increases of plasma concentrations of very low density lipoproteins were due to an increase in the rate of synthesis or a decrease in the rate of clearance of these particles, the metabolism of radiolabeled homologous very low density lipoproteins was studied during intravenous infusion of immunoglobulin G prepared from the antisera against hepatic triglyceride lipase (n = 3) or preimmune goat sera (n = 3). Studies performed in the same animals during saline infusion were used as controls for each immunoglobulin infusion. There was a twofold increase in the apparent half-life of the very low density lipoprotein apolipoprotein-B tracer in animals receiving the antibody, consistent with a decreased catabolism of very low density lipoproteins. Concomitantly, the rise in low density lipoprotein apoprotein-B specific activity was markedly delayed. None of these changes were observed during infusion of preimmune immunoglobulin G.Hepatic triglyceride lipase participates with lipoprotein lipase in the hydrolysis of the lipid in very low density lipoproteins, intermediate density lipoproteins, and the larger low density lipoproteins (S(f) 9-12). Thus, hepatic triglyceride lipase appears to function in a parallel role with lipoprotein lipase in the conversion of very low density and intermediate density lipoproteins to low density lipoproteins (S(f) 0-9).

Metabolic disorders of serum lipoproteins in endotoxin-poisoned mice: the role of high density lipoprotein (HDL) and triglyceride-rich lipoproteins.

A study was performed to clarify the role of serum lipoproteins, especially high density lipoprotein (HDL) and triglyceride-rich lipoproteins in endotoxemic or endotoxin-poisoned animals. The level of HDL-cholesterol decreased markedly in mouse serum 18-24 hr postintoxication, while the amount of low density lipoprotein (LDL)-cholesterol in the sera of poisoned mice was about 175% of that of the controls. Serum lecithin-cholesterol acyltransferase activity in the poisoned mice decreased slightly for 3-6 hr after endotoxin injection, but became markedly increased at 18-24 hr as compared with that in the controls. The amount of serum very low density lipoprotein (VLDL) showed a marked increase in the poisoned mice 8-24 hr postintoxication. The HDL fraction in the electrophoretic patterns of serum was reduced according to the dose of endotoxin 18 hr postintoxication. The HDL fraction in mice injected with lead acetate plus endotoxin was markedly lower than that in the poisoned mice. When streptozotocin-diabetic mice were injected with endotoxin, the HDL fraction was higher than that in the endotoxin-poisoned mice. In endotoxin-poisoned mice a correlation was observed between the lipid peroxide and LDL levels in the serum. In disk electrophoretic patterns, the HDL fraction in mice given vitamin E-supplemented diet showed a higher level than that in mice given a normal diet. Lipoprotein lipase (LPL) activity in poisoned mice significantly decreased to 59% of the control value 18 hr postintoxication, but hepatic triglyceride lipase activity was only slightly increased in endotoxin-poisoned mice. In analysis of HDL apoprotein peptide in serum lipoprotein, the apo C-II peptide level was clearly lower in mouse serum 18 hr postintoxication than that in the controls. These results suggest that the decrease in LPL activity in endotoxin-poisoned mice may be closely related to a decrease in the apo C-II peptide level, and also that it plays an important part in HDL and triglyceride-rich lipoprotein metabolism in the poisoned mice.

The storage and synthetic pools of heparin-releasable lipoprotein lipase and hepatic triacylglycerol lipase in the growing puppy.

Age-related changes in the activities of extrahepatic lipoprotein lipase and hepatic triacylglycerol lipase were determined during a primed/constant-rate infusion of heparin for 2 h in puppies between birth and 18 weeks of age. The early (storage) and late (synthetic) phases were measured. Both phases of hepatic triacylglycerol lipase activity were well developed in the first week, reflecting the metabolic maturity of the liver at birth. During the 18 weeks of study, the activity remained relatively unchanged except for a sharp peak at 12 weeks. Extrahepatic lipoprotein lipase activity was low in the first 4 weeks of suckling. Its storage pool increased 6-fold in the next 14 weeks, with a less marked rise in its late (synthetic) pool. Sustained increases in the activity of this enzyme were first noticed during weaning, when the insulin-secretory response matured. Endogenous insulin-secretory capacity rather than the fat content of the feed appeared significant in the postnatal development of lipoprotein lipase (Clearing-factor lipase) activity.

Roles of lipoprotein lipase and hepatic triglyceride lipase in the catabolism in vivo of triglyceride-rich lipoproteins.

To define the roles, in vivo, of hepatic triglyceride lipase and lipoprotein lipase in the catabolism of triglyceride-rich lipoproteins, we investigated the relationship between the activities of the above enzymes in postheparin plasma and the fractional removal rates of very low density lipoproteins (VLDL) and VLDL remnant particles. In 22 patients, the fractional removal rates of VLDL and VLDL-remnant particles were determined from analyses of the disappearance of radioiodinated Sf 60-400 and Sf 12-60 lipoprotein B apoprotein. The maximal activities of hepatic triglyceride lipase and lipoprotein lipase were determined in plasma samples drawn 2-60 minutes after heparin injection (60 U/kg). A positive correlation was observed between the fractional removal rate of VLDL and postheparin plasma lipoprotein lipase activity (r = 0.65). When all 22 patients were considered together, no relationship was demonstrable between remnant fractional removal and postheparin plasma lipoprotein lipase activity. However, humans may be subdivided with respect to the way in which they catabolize remnants. In some, all remnant may be catabolized to form LDL. In others, some of the remnant may also be directly removed from the circulation. Those subjects in whom previous studies indicate that all remnant is converted to LDL demonstrated a positive correlation between remnant fractional removal rate and postheparin plasma lipoprotein lipase activity (n = 8, r - 0.83). No correlations between postheparin plasma hepatic triglyceride lipase activity and any of the fractional removal rates were found. These data are consistent with the following: 1) lipoprotein lipase plays a key regulatory role in the catabolism of triglyceride-rich lipoproteins; 2) this role applies only to those catabolic involving the formation of particles of higher density VLDL remnants and low density lipoprotein; and 3) hepatic triglyceride lipase plays no rate-limiting role in the catabolism of VLDL or VLDL-remnant particles.

The effects of fasting and streptozotocin diabetes on the triglyceride lipase activity of rat liver plasma membranes.

AbstractThe activity of hepatic triglyceride lipase (H‐TGL) of plasma membranes isolated from rat liver is shown to be reduced by fasting. Refeeding restores the enzyme activity. The suppressed activity of H‐TGL in streptozotocin diabetic rats is restored by insulin treatment. The behavior of the enzyme activites in both situation coincides with that of plasma insulin levels. The results suggest that the H‐TGL of rat liver plasma membranes is under hormonal regulation by insulin.

Effects of threonine-poor apolipoproteins on post-heparin plasma hepatic triacylglycerol lipase and lipoprotein lipase

Whole-irradiated rabbit pre-heparin plasma had an important inhibitory effect on hepatic triacylglycerol lipase and lipoprotein lipase activities, whereas control rabbit pre-heparin plasma slightly inhibited hepatic triacylglycerol lipase activity at a high concentration and enhanced lipoprotein lipase activity. As some apolipoproteins were known to modulate these two lipolytic enzymes, the inhibitory effects of irradiated rabbit plasma were investigated in apolipoproteins. Three apolipoproteins, with isoelectric points of about 6.58, 6.44 and 6.12, characterized by their low content in threonine (threonine-poor apolipoproteins) were produced in high concentrations in rabbit VLDL and HDL after irradiation. The effects of these apolipoproteins on control rabbit post-heparin plasma hepatic triacylglycerol lipase and extrahepatic lipoprotein lipase were studied. Threonine-poor apolipoproteins substantially inhibited the hepatic triacylglycerol lipase activity and enhanced the apolipoprotein C-II-stimulated activity of lipoprotein lipase. The amounts of these apolipoproteins in triacylglycerol-rich lipoprotein particles may determine the lipolytic activity of lipoprotein lipase and hepatic triacylglycerol lipase in triacylglycerol hydrolysis. The existence of another inhibitor of lipoprotein lipase remains to be determined.

The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.

Hepatic triacylglycerol lipase activities after induction of diabetes and administration of insulin or glucagon.

Triacylglycerol lipase activities of homogenates and subcellular fractions of rat liver were measured under optimal conditions at pH 7.5 using emulsified tri[1-14C]oleoylglycerol as substrate. Twenty-four hr after administration of streptozotocin, hepatic alkaline lipase activity was 39% of normal, and this lower level of activity was observed at 72 hr and 7 days, after streptozotocin injection. After 24 hr of starvation, lipase activity also was significantly lower (35%) than normal. Insulin (35 U regular/kg body weight) had no acute (90 min) effect on the hepatic lipase activity of either normal or diabetic rats. Chronic insulin administration (4 subcutaneous injections of 10 U protamine zinc insulin/kg at 16-hr intervals) to normal rats provoked a 40% increase in hepatic lipase activity. Diabetic rats given the same insulin treatment showed lipase activity that was significantly higher (155%) than normal. Lipase activity fell to 65% of normal when insulin was withheld (32 hr) from diabetic rats given chronic insulin therapy. Intracardial injection of glucagon (1 mg/kg) into normal rats had no acute (30 min) effect on hepatic alkaline lipase activity. Hepatic alkaline lipase activity varied independently from the concentrations of either glucose or triacylglycerol in the plasma. However, there was an apparent negative correlation between this lipase activity and the concentration of fatty acids in the plasma; lipase activity was highest when fatty acid concentrations were lowest, and lowest when fatty acid concentrations were elevated. From these data we conclude: 1) changes in hepatic alkaline lipase activity ware provoked by chronic, but not acute, alteration of the hormonal and metabolic status of the rat, and 2) changes in hepatic alkaline lipase activity may be mediated through changes in the levels of circulating fatty acids presented to the liver, but the effect is not an immediate one.

Plasma lipoprotein lipase and hepatic lipase activities in Friedreich's ataxia.

Plasma triglycerides although within the normal range have been shown to be higher in Friedreich's ataxia than in control subjects. To determine whether this difference could be ascribed to a reduced catabolism of triglyceride-rich lipoproteins, the activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HL), released into plasma after an heparin injection, were measured in 13 cases of Friedreich's ataxia and 14 control subjects of comparable signs. LPL was found to be significantly lower in the ataxic patients. Moreover about half of the cases clustered below the normal range for both lipase activities. This subgroup of Friedreich's patients had significantly higher plasma triglycerides than those with normal lipase activities. Further studies are needed to relate these findings to other characteristics of the disease.

低HDL血症患者のHDL代謝における肝性トリグリセリドリパーゼの役割

It has been indicated that lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) play a role not only in the metabolism of triglyceride rich lipoproteins but also in HDL metabolism. The purpose of the present study was to investigate the role of LPL and H-TGL in the metabolism of HDL-subfractions, HDL2 and HDL3 in the subjects with hypo-high density lipoproteinemia. Clinical diagnosis of the 29 patients with hypohigh density lipoproteinemia studied in the present study were postapoplexy in the steady state, coronary heart disease and hypertension etc. Furthermore, seventeen hypo-high density lipoproteinemia with diabetes mellitus, 19 subjects with normal levels of HDL-cholesterol (C) and 8 diabetics with normal levels of HDL-C were studied. Hypo-high density lipoproteinemia was defined by (HDL2+HDL3)-cholesterol less than 40mg/100ml. Plasma lipoproteins were fractionated by sequential ultracentrifugation at densities 1.063 and 1.110g/ml to obtain VLDL+LDL(d<1.063g/ml), HDL2(1.063<d<1.110g/ml) and HDL3 (d>1.110g/ml). Concentrations of cholesterol, triglyceride and phospholipid in plasma and each lipoprotein fraction were measured. Activities of LPL and H-TGL in postheparin plasma obtained 10min after injection of heparin, 10U/Kg body weight, were assayed utilizing the substrate containing [14C] triolein. Separate assay of LPL and H-TGL activities were performed by inhibition of LPL activity by 1M NaCl. Cholesterol concentrations in HDL2 and HDL3 from hypohigh density lipoproteinemia were significantly lower than those from the patients with normal levels of HDL-C. Decrease of HDL2-cholesterol was more remarkable than that of HDL3-cholesterol. Therefore, HDL2-Ch/HDL3-Ch ratio was significantly lower in hypo-high density lipoproteinemia than in the patients with normal levels of HDL-Ch. As far as phospholipid is concerned, the same tendency was observed as cholesterol. There was no significant difference in triglyceride concentration in HDL2 and HDL3 between hypo- and normo-high density lipoproteinemia. LPL activity was significantly lower in hypo-high density lipoproteinemia without diabetes mellitus than in normo-high density lipoproteinemia. There were no significant differences in H-TGL activities among 4 groups. In hypo-high density lipoproteinemia, significantly negative correlations were observed between H-TGL activities and concentrations of cholesterol and phospholipid in HDL2. Significantly positive correlations were observed between LPL activities and concentrations of triglyceride and phospholipid in HDL2. However, there were no significant correlations among LPL activity, H-TGL activity and lipids concentrations in HDL3. These correlations were much more obvious in diabetics with hypo-high density lipoproteinemia. The data presented indicate the important role of LPL and H-TGL in the metabolism of HDL2 and HDL3 in the subjects with hypo-high density lipoproteinemia.

Purification, stabilization, and characterization of rat hepatic triglyceride lipase

Hepatic triglyceride lipase (H-TGL) was purified to near homogeneity from heparin-containing rat liver perfusates with the following column chromatography steps: heparin-Sepharose affinity chromatography, anion-exchange chromatography on DEAE-Sephacel, and gel filtration on Ultrogel AcA 34. A final specific activity of 45,000 μmol fatty acid/mg/h was obtained with an overall 31% recovery of catalytic activity. The heparin-Sepharose step resulted in a 20-fold purification, while the DEAE and gel filtration steps led to further purification with complete recovery of activity. An extensive survey of various detergents as potential stabilizers of H-TGL activity led to the selection of Triton N-101 for use in the column buffers of the DEAE and gel filtration steps. Relative to initial H-TGL activity upon dilution in buffer without detergent, recoveries between 90 and 100% were consistently obtained with Triton N-101-containing buffers following a 24-h incubation at 20°C. In contrast after a 24-h incubation at 20°C those control samples lacking detergent were at least 95% inactivated. The highly purified H-TGL exhibited a single major band by sodium dodecyl sulfate-electrophoresis. The use of DEAE chromatography and stabilization of H-TGL with Triton N-101 are the improvements in purification that resulted in an 8-fold enhancement in specific activity relative to the highest previous report of purification from rat liver perfusates.

Apo A-I and Apo A-II inhibit hepatic triglyceride lipase from human postheparin plasma

Summary The effect of apolipoprotein A-I and A-II on hepatic triglyceride lipase activity was studied. Purification of apolipoprotein A-I and A-II was carried out by gel filtration with Sephadex G-200 in 6 M urea. Hepatic triglyceride lipase was purified from human postheparin plasma by heparin-Sepharose affinity chromatography. We demonstrated that both apolipoprotein A-I and A-II substantially inhibited hepatic triglyceride lipase. It suggests that these apolipoproteins play an important role in the inhibition of hepatic triglyceride lipase activity by whole serum.

A selective decline of postheparin plasma hepatic triglyceride lipase in hypothyroid rats

The present study aimed to define the effect of thyroid status on two postheparin plasma lipases, i.e., lipoprotein lipase and hepatic triglyceride lipase. Rats with hypo- and hyperthyroidism were used for this purpose. Separate measurement of these two lipases was done by an immunochemical method utilizing antiserum specific to hepatic triglyceride lipase. The 5-wk thyroidectomized, hypothyroid rats had normal plasma concentrations of both triglyceride and cholesterol. These rats showed a selective decline in the activity of postheparin plasma hepatic triglyceride lipase with normal lipoprotein lipase activity. The rats made thyrotoxic by thyroxine treatment had normal plasma levels of both triglyceride and cholesterol. These rats showed normal activities of both hepatic triglyceride lipase and lipoprotein lipase. The observed finding of a selective decline of hepatic triglyceride lipase in hypothyroid rats is discussed in connection with the possible function of this enzyme in lipoprotein metabolism.

Specific modification of hepatic triglyceride lipase activity by ultracentrifugally separated serum lipoprotein fractions.

Hepatic triglyceride lipase (H-TGL) obtained from postheparin plasma is first stimulated and than progressively inhibited by addition of an increasing amount of serum. To solve the mechanism of this modification, serum fractions isolated by ultracentrifugation were added to the assay mixture and their effects on H-TGL activity were determined. We demonstrated that the addition of the d=1.21 bottom fraction together with HDL almost fully reproduces the effect of the whole serum.

Decline of postheparin plasma lipoprotein lipase in acromegalic patients

Lipoprotein lipase and hepatic triglyceride lipase in postheparin plasma were measured in seven patients with active acromegaly by an immunochemical method utilizing antiserum prepared against hepatic triglyceride lipase. A mild or moderate hypertriglyceridemia was shown, with plasma triglyceride concentrations between 156 and 544 mg/dl. Lipoprotein lipase was found to be decreased in all patients ( p < 0.001). Hepatic triglyceride lipase was also low in these patients ( p < 0.001). We speculate that acromegalic hypertriglyceridemia is mediated, at least in part, by the decline in lipoprotein lipase and possibly by the decline in hepatic triglyceride lipase activities.

Oral levo-norgestrel — Testosterone effects on spermatogenesis, hormone levels, coagulation factors and lipoproteins in normal men

Four healthy men volunteered to be treated for eight to nine months with daily oral levo-norgestrel (250 <g) and oral testosterone (200–600 mg) as a possible contraceptive. This was followed by a recovery phase of 5–10 months. The oral steroid combination significantly decreased sperm count in 3 of 4 subjects, and significantly increased abnormal spermatozoa, serum LH was decreased during treatment but serum FSH remained constant, except for one volunteer. Serum testosterone was decreased except for 2 daily peaks associated with the oral testosterone. During the recovery period, sperm counts and morphology, serum testosterone and serum LH returned to normal, whereas serum FSH levels were increased. Platelet aggregability induced by ADP, increased in 3 volunteers during treatment as did fibrinolytic activity and fibrinolytic capacity (2 of 3 subjects). There was a reduction in the hepatic triglyceride lipase activity but no change was seen in serum triglycerides, serum cholesterol, serum LDL, serum HDL, peripheral lipoprotein lipase activity and the intravenous fat tolerance test. No other toxicological side effects were seen.

Hyperlipoproteinemia in renal insufficiency.

In uremic patients, hyperlipoproteinemia is common, but its role as a risk factor in atherogenesis remains controversial. The main abnormality appears to be diminished catabolism of lipoproteins in the face of unchanged or low hepatic synthesis. The relation of diminished catabolism to reduced postheparinlipolytic activity and selective deficiency of hepatic triglyceride lipase remains to be established. Hyperlipoproteinemia in uremic patients, most commonly of the type IV variety, responds to dietary methods (reduction of carbohydrate content, increase in P/S ratio) or pharmacological intervention. Guidelines for therapy remain controversial in view of the uncertainty about the pathogenic role of hyperlipoproteinemia in atherogenesis.

Increase in Lipoprotein Lipase during Clofibrate Treatment of Hypertriglyceridemia in Patients on Hemodialysis

In 11 hypertriglyceridemic patients on hemodialysis, clofibrate (1 to 1.50 g per week) reduced plasma triglyceride (-40 +/- 20%, P less than 0.001), very-low-density-lipoprotein triglyceride (-44 +/- 20%, P less than 0.001) and very-low-density lipoprotein cholesterol (-39 +/- 25%, P less than 0.01), and it increased high-density-lipoprotein cholesterol (82 +/- 106%, P less than 0.005). Low pretreatment lipoprotein-lipase activity in adipose-tissue specimens and postheparin plasma increased to normal with clofibrate, whereas low hepatic triglyceride lipase activity did not change. The reduced very-low-density-lipoprotein triglyceride correlated with the increased lipoprotein-lipase activity in adipose tissue (rs = 0.792, P less than 0.02, n = 8) and postheparin plasma (rs = 0.851, P less than 0.02, n = 8), whereas increased high-density-lipoprotein cholesterol correlated with changes in this activity in adipose tissue (rs = 0.696, P less than 0.06) and post-heparin plasma (rs = 0.679, P less than 0.10). There was no correlation between changes in hepatic triglyceride lipase activity and plasma lipids during treatment. Reduced lipoprotein-lipase activity may cause hypertriglyceridemia and decreased high-density-lipoprotein cholesterol in patients on hemodialysis; clofibrate may correct these abnormalities by increasing lipoprotein-lipase activity to normal.