Effect of fasting on two postheparin plasma triglyceride lipases and triglyceride removal in obese subjects.

A new method was used for selective measurement of lipoprotein lipase and hepatic lipase in human postheparin plasma. Hepatic lipase was assayed in 1.0 M NaCl withour addition of serum, and the activity of lipoprotein lipase was determined in 0.1 M NaCl after immunoprecipitation of hepatic lipase with specific antiserum. The activity of both these enzymes and the total lipolytic activity were measured in plasma samples taken during a 4-h infusion of heparin. Each of the activities was related to basal serum triglyceride concentration and to the fractional removal constant (K) of Intralipid in 13 obese subjects before and after prolonged fasting. During a normal isocaloric diet the lipolytic activities showed a biphasic response to heparin infusion in all subjects. A peak activity was reached within 30 minutes ("early response") and thereafter the lipase activities decreased to a constant level maintained during the rest of the heparin infusion ("late response"). The early response of lipoprotein lipase showed a significant inverse correlation with the basal serum triglyceride level (r = -0.85) and a significant positive correlation with the fractional removal rate of Intralipid (r = 0.84). The late response of lipoprotein lipase was not related to either of these parameters. The early response of hepatic lipase was not correlated with basal triglyceride concentration or Intralipid removal, whereas the late response of this enzyme showed a significant negative correlation with the removal rate of Intralipid (r = -0.82). After fasting for several days the acute response of all lipolytic activities to heparin was markedly decreased or totally abolished, but the magnitude of the late response was similar to that seen in the fed state. The fractional removal rate of Intralipid was slightly increased by starvation. All correlations between postheparin plasma lipases and serum triglyceride concentration and removal disappeared in fasting subjects. It is concluded that the rapidly releasable lipoprotein lipase probably reflects the activity of the tissue enzyme(s) which is responsible for the primary removal of very low density lipoprotein (VLDL) triglycerides and chylomicrons. It is probable that this component of the postheparin plasma lipolytic activity is derived from the endothelial lipoprotein lipase pool. This enzyme plays a key role in the efflux of plasma triglycerides under normal conditions, and it is thus one determinant of plasma triglyceride level. Prolonged fasting obviously changes the triglyceride removal sites and mechanism but does not impair the removal efficiency.     

Effect of Fasting on Two Postheparin Plasma Triglyceride Lipases and Triglyceride Removal in Obese Subjects

Abstract. A new method was used for selective measurement of lipoprotein lipase and hepatic lipase in human postheparin plasma. Hepatic lipase was assayed in 1. 0 M NaCl without addition of serum, and the activity of lipoprotein lipase was determined in 0. 1 M NaCl after immunoprecipitation of hepatic lipase with specific antiserum. The activity of both these enzymes and the total lipolytic activity were measured in plasma samples taken during a 4-h infusion of heparin. Each of the activities was related to basal serum triglyceride concentration and to the fractional removal constant (K) of Intralipid in 13 obese subjects before and after prolonged fasting. During a normal isocalqric diet the lipolytic activities showed a biphasic response to heparin infusion in all subjects. A peak activity was reached within 30 minutes (“early response”) and thereafter the lipase activities decreased to a constant level maintained during the rest of the heparin infusion (“late response”). The early response of lipoprotein lipase showed a significant inverse correlation with the basal serum triglyceride level (r – 0. 85) and a significant positive correlation with the fractional removal rate of Intralipid (r + 0. 84). The late response of lipoprotein lipase was not related to either of these parameters. The early response of hepatic lipase was not correlated with basal triglyceride concentration or Intralipid removal, whereas the late response of this enzyme showed a significant negative correlation with the removal rate of Intralipid (r = - 0. 82). After fasting for several days the acute response of all lipolytic activities to heparin was markedly decreased or totally abolished, but the magnitude of the late response was similar to that seen in the fed state. The fractional removal rate of Intralipid was slightly increased by starvation. All correlations between postheparin plasma lipases and serum triglyceride concentration and removal disappeared in fasting subjects. It is concluded that the rapidly releasable lipoprotein lipase probably reflects the activity of the tissue enzyme(s) which is responsible for the primary removal of very low density lipoprotein (VLDL) triglycerides and chylomicrons. It is probable that this component of the postheparin plasma lipolytic activity is derived from the endothelial lipoprotein lipase pool. This enzyme plays a key role in the efflux of plasma triglycerides under normal conditions, and it is thus one determinant of plasma triglyceride level. Prolonged fasting obviously changes the triglyceride removal sites and mechanism but does not impair the removal efficiency.     

Effect of parenteral hyperalimentation on serum lipoproteins and on lipoprotein lipase activity of adipose tissue and skeletal muscle

This study reports on the effects of parenteral nutrition with glucose along or in combination with Intralipid on heparin-releasable lipoprotein lipase (LPL) activity of adipose tissue and skeletal muscle and on serum lipoproteins. Thirteen patients with postoperative hypercatabolism and nine patients with caloric malnutrition were studied. The average adipose tissue LPL activity increased 5-fold during 4-day glucose infusion (P less than 0.001) and 7.4-fold during Intralipid plus glucose infusion (P less than 0.001). In contrast, no change occurred in the LPL activity of skeletal muscle. Glucose infusion caused a significant increase in VLDL and LDL triglyceride concentrations and the Intralipid plus glucose infusion was followed by a rise in LDL and HDL triglyceride concentrations. HDL cholesterol decreased by 26% (P less than 0.01) during glucose and by 19% (P less than 0.05) during Intralipid plus glucose. Apoprotein A I was very low already at the start of parenteral alimentation and it did not change during either nutrition. The HDL cholesterol and apoprotein A I and A II levels were each positively correlated with adipose tissue LPL activity before parenteral nutrition but not after it.     

Lipolytic and anticoagulant activities of a low molecular weight fragment of heparin

Low molecular weight heparin (LMWH) and standard heparin were given intravenously to six healthy subjects receiving a continuous infusion of Intralipid. After infusion, antifactor Xa, antithrombin II and coagulation activity (Normotest) were the same for both heparins. Activated partial thromboplastin time increased significantly, but the increase was much higher after standard heparin (+473%) than after LMWH (+48%). The increase in lipoprotein lipase activity was less pronounced after LMWH infusion. This resulted in a smaller decrease in Intralipid-triglyceride concentration and a smaller increase in both plasma FFA concentration and Intralipid fractional removal rate compared to standard heparin. This study shows that the plasma lipolytic potential of LMWH is weaker than that of standard heparin when given in doses with equipotent anticoagulation. LMWH may therefore be preferable to standard heparin as an antithrombotic agent in clinical situations where a high plasma lipolytic activity may be disadvantageous.     

Evaluation of the roles of lipoprotein lipase and hepatic lipase in lipoprotein metabolism: in vivo and in vitro studies in man

Abstract. The roles of lipoprotein lipase (LPL) and hepatic lipase in very low density lipoprotein (VLDL) and VLDL remnant metabolism were investigated by (1) in vivo studies where the kinetics of VLDL-apo B removal were measured in patients with non-functioning lipoprotein lipase systems, and (2) in vitro studies where the relative capacities of hepatic lipase and LPL to hydrolyse the triglyceride (TG) of different lipoprotein substrates was measured. The results indicated that VLDL-apo B removal was not impaired in patients with non-functional LPL, nor was there any apparent abnormality in the conversion of VLDL-apo B to intermediate- (IDL) and low (LDL) density lipoprotein-apo B. Post-heparin plasma hepatic lipase activity against VLDL was normal in these subjects. Purified normal hepatic lipase had a similar K_m for VLDL-TG hydrolysis (1.57 mmol/l) to that of LPL (1.49 mmol/l). However, at equal lipoprotein TG concentration, hepatic lipase had increasing activity with lipoproteins of decreasing particle size, in the order chylomicrons ≪ VLDL of Sf 100–400 < VLDL of Sf 60–100 < VLDL of Sf 20–60 < IDL. The mean contribution of hepatic lipase to VLDL-TG hydrolysis by post-heparin plasma was 35% in normal controls, but the contribution to IDL-TG hydrolysis was significantly higher (mean = 58%). It is concluded that hepatic lipase plays a significant role in VLDL and, especially, IDL metabolism, at least in patients with non-functioning lipoprotein lipase.     

Different types of heparin in haemodialysis: Long-term effects on post-heparin lipases

Several long-term studies of haemodialysis patients have shown improved serum lipid profile associated with treatment with low molecular weight heparin (LMWH) as compared with unfractionated heparin (UH). This has been attributed to the fact that LMWH produces a less marked acute lipolytic response than UH. However, the information on the differences in long-term effects on tissue releasable Upases is limited. Post-heparin plasma lipase activities were measured at 6, 24 and 48 h after pre-dialysis heparin injections in seven patients on chronic haemodialysis during treatment with UH; these measurements were then repeated 2 and 6 months after treatment was switched to LMWH. The curves plotted from the results can be assumed to reflect the interdialytic lipolytic potential. In the case of lipoprotein lipase this was unchanged 2 months after treatment was switched from UH to LMWH but increased by a mean of 47% after 6 months. In the case of hepatic lipase there was no change in the interdialytic lipolytic potential. Thus, there was a slow increase in tissue releasable lipoprotein lipase stores after treatment was switched from UH to LMWH, probably reflecting a smaller loss of lipoprotein lipase after each LMWH injection. Hepatic lipase, in contrast, was not affected by the type of anticoagulation.     

Effect of medium- and long-chain triglyceride infusion on lipoprotein and hepatic lipase in healthy subjects

Plasma lipolytic activity and hydrolysis of intravenous fat were studied in six healthy subjects during infusion of a long-chain triglyceride (LCT) fat emulsion (Intralipid 20%) or of a medium-chain triglyceride (MCT)/LCT emulsion (Lipofundin MCT 20%). The fat emulsions were infused continuously at a rate of 0.17 g triglyceride kg-1 body weight (BW)h-1 for 6 h in random order at 7-day intervals. A continuous infusion of glucose (0.18 g kg-1 BW h-1) was administered for a period of 7 h and was started 1 h before the lipid infusion. Infusions of both types of fat increased plasma triglyceride (TG), free fatty acid (FFA) and lipoprotein lipase (LPL) levels and steady-state values were present during the 3rd to 5th h of infusion. MCT/LCT infusion resulted in higher plasma levels at steady-state of TG (3.63 +/- 0.45 [SEM] vs 2.73 +/- 0.45 mmol l-1; P less than 0.05), FFA (1.05 +/- 0.08 vs 0.54 +/- 0.04 mmol l-1; P less than 0.01) and LPL (4.6 +/- 0.6 vs 2.6 +/- 0.5 mU ml-1; P less than 0.05) in comparison with LCT administration. There was a positive correlation between plasma LPL activity and TG concentration (r = 0.77; P less than 0.001) when data for the two infusions were combined. Although the same amount of fat was infused on a weight basis, the molar infusion rate was 40% higher with MCT/LCT than with LCT infusion, due to differences in molecular weights (634 vs 885 Da).(ABSTRACT TRUNCATED AT 250 WORDS)     

Familial apolipoprotein CII deficiency: plasma lipoproteins and apolipoproteins in heterozygous and homozygous subjects and the effects of plasma infusion

Abstract. Plasma lipoproteins and apolipoproteins have been studied in a kindred with familial apolipoprotein CII (apo CII) deficiency. As in two other recently documented pedigrees, apo CII deficiency appeared to be transmitted as an autosomal recessive trait. The homozygous state was characterized by gross fasting hypertriglyceridaemia, complete absence of apo CII from plasma and failure of plasma to activate lipoprotein lipase. Post-heparin plasma hepatic triglyceride lipase activity was normal. Hypertriglyceridaemia reflected chylomicronaemia and elevated Sf 100–400 and Sf 20–100 lipoprotein concentrations; lipoproteins of Sf 12–20 (LDL₁), Sf 0–12 (LDL₂), F_1.23.5–9 (HDL₂) and F_1.20–3.5 (HDL₃) were greatly reduced in concentration. Low density lipoproteins (1.006–1.063 g/ml), isolated by preparative ultracentrifugation, and high density lipoproteins, isolated by heparin/Mn⁺⁺, were triglyceride-enriched. Electroimmunoassays revealed additionally low plasma concentrations of apolipoproteins AI, AII and B and very high concentrations of apolipoproteins CIII and E in the homozygote. The parents of the proband (heterozygotes) were normotriglyceridaemic, and had normal lipoprotein lipid concentrations and normal apolipoprotein AI, AII, B, CIII and E concentrations, in spite of having low apo CII concentrations. Activation of lipoprotein lipase in the homozygote by intravenous infusion of 200 ml fresh-frozen plasma rapidly reduced the plasma concentrations of chylomicrons and very low density lipoproteins (VLDL). Within VLDL, the decrease in concentration occurred sequentially in the Sf 100–400 and Sf 20–100 subclasses. These changes were associated during a 4-day study period with reciprocal increases in LDL₁, LDL₂, HDL₂ and HDL₃. The plasma concentrations of apo AI and apo B also increased, associated with a less marked fall in that of apo CIII; the apo AII and apo E concentrations were unchanged. These observations support other evidence that apo CII is a cofactor for the catabolism of chylomicrons and both major subfractions of VLDL by lipoprotein lipase in man, and that human LDL₁ and LDL₂ are derived, at least in part, from triglyceride-rich lipoprotein catabolism. They also suggest that both major subfractions of HDL acquire additional components during triglyceride-rich lipoprotein catabolism. In normal subjects the plasma apo CII concentration appears to be greatly in excess of that required for adequate activation of lipoprotein lipase.     

Relationships between the metabolism of high-density and very-low-density lipoproteins in man: studies of apolipoprotein kinetics and adipose tissue lipoprotein lipase activity

Abstract. In order to gain further insight into the relationship between high-density lipoprotein (HDL) metabolism and plasma triglyceride transport, measurements were made of HDL cholesterol concentration, apoprotein (apo) AI and AII metabolism, very-low-density lipoprotein (VLDL) apo B metabolism, and heparin-elutable adipose tissue lipoprotein lipase (LPL) activity in seventeen subjects with a wide range of plasma triglyceride concentrations (0.8–25 mmol/l).
The fractional catabolic rate (FCR) of VLDL apo B was directly related to LPL activity ( r =+ 0.80), providing evidence that the activity of the enzyme in adipose tissue is a determinant of the rate of lipolysis of VLDL in man. HDL cholesterol concentration was a positive function of both VLDL apo B FCR ( r =+ 0.74) and LPL activity, a finding consistent with previous evidence for the origin of a proportion of HDL cholesterol from 'surface remnants' liberated during VLDL catabolism. The FCRs of both apo AI and apo AII were inversely related to VLDL apo B FCR (AI, r = - 0.52; AII, r = - 0.69) and to LPL activity. The synthetic rate of apo AII, but not that of apo AI, was positively correlated with VLDL apo B synthesis ( r =+ 0.71). Thus, the metabolism of the major proteins of HDL in man appears to be closely associated with VLDL metabolism.     

Lower plasma levels of lipoprotein lipase after infusion of low molecular weight heparin than after administration of conventional heparin indicate more rapid catabolism of the enzyme

The functional pool of lipoprotein lipase (LPL) is anchored to heparan sulfate at the vascular endothelium. Injection of heparin releases the enzyme into the circulating blood. Animal experiments have shown that the enzyme is then extracted and degraded by the liver. Low molecular weight (LMW) heparin preparations are widely used in the clinic and are supposed to release less LPL. In this study, we infused a LMW heparin into healthy volunteers for 8 hours. The peak of LPL activity was only about 30% and the subsequent plateau of LPL activity only about 40% compared with those seen with conventional heparin. When a bolus of heparin was given after 4 hours' infusion of LMW or conventional heparin, only relatively small, and similar, amounts of LPL entered plasma. This suggests that the difference between LMW and conventional heparin lay in the ability to retain LPL in the circulating blood, not in the ability to release the lipase. Triglycerides (TGs) decreased when the heparin infusion was started, as expected from the high circulating LPL activities. After 1 to 2 hours, TG levels increased again, and after 8 hours they were about twice as high as before the heparin infusion. This indicates that the amount of LPL available for lipoprotein metabolism had become critically low in relation to TG transport rates. This study indicates that LMW heparin compared with conventional heparin causes as much or more depletion of LPL and subsequent impairment of TG clearing.     

Serum lipoprotein lipase mass: clinical significance of its measurement

Lipoprotein lipase (LPL) is a lipolytic enzyme involved in catalyzing hydrolysis of triglycerides (TG) in chylomicrons and very low-density lipoprotein (VLDL) particles. Over the last decade, increasing attention has been paid to the clinical significance of measuring serum LPL protein mass without heparin injection to the study subjects. In earlier studies, this marker was utilized to classify LPL deficient subjects, which is an extremely rare metabolic disorder with a frequency of one in one million. Later, researchers paid more attention to the clinical significance of measuring this parameter in more common metabolic disorders. Studies have shown that pre-heparin plasma or serum LPL mass has significant relationships with serum lipids and lipoproteins, visceral fat area, insulin resistance, and even the development of coronary atherosclerosis in cross-sectional studies, although this might be a metabolic surrogate marker with almost no catalytic activities, which does not appear to be involved in catalyzing hydrolysis of TG in TG-rich lipoproteins. Recently, a prospective study has demonstrated that low serum LPL concentration predicts future coronary events. Taken together, we suggest that pre-heparin LPL mass in plasma or sera provide us with useful and important information on the development of metabolic disorders leading to atherosclerotic disease.     

A micromethod for assay of lipoprotein lipase activity in needle biopsy samples of human adipose tissue and skeletal muscle

A rapid and simple procedure for assay of lipoprotein lipase (LPL) activity in small amounts of human adipose tissue and skeletal muscle is described and validated. The enzyme is eluted from tissues with heparin and the activity is determined from the eluate by measuring the release of [¹⁴C]oleic acid from a gum arabic stabilized emulsion of glycerol-tri[¹⁴C]oleate in a Tris-buffer medium containing albumin and pooled normal human serum. Reproducible results are obtained with amounts of tissue ranging from 2 to 25 mg.The K_m values of the adipose tissue and skeletal muscle LPL for the triolein substrate were 0.74 ± 0.06 and 0.77 ± 0.05 mmol/l, respectively. The standard radioactive triolein emulsion was hydrolyzed by adipose tissue LPL at a rate closely similar to rat VLDL-triglyceride labeled in vivo with [1-¹⁴C]palmitic acid, suggesting that the experimental substrate behaved in a similar manner to the natural substrate. The LPL activity was much higher in adipose tissue than in muscle. In adipose tissue the LPL activity was 2–4 times higher in women than in men whereas no sex difference was present in the LPL activity of muscle.     

Differences in heparin-released lipolytic activity in the superficial and deep veins of the human forearm

Various doses of heparin were given as a single injection into the brachial artery of each of twelve fasting healthy males. Plasma lipolytic activity was measured in samples obtained before and at frequent time intervals after heparin injection, in the artery and the deep and superficial veins of the same forearm. As little as 0.15 U heparin produced a rapid and detectable release of lipolytic activity in both deep and superficial veins. A series of tenfold increases in the dose produced correspondingly greater releases in the veins but the increments in the release were smaller than the increments in the dose. Three repeated 15 U doses of heparin, separated by 30 min, in the same subject gave a high degree of reproducibility of the release of lipolytic activity in both deep and superficial veins. 90% of the lipase activity in the vein was inhibited by 1 M NaCl. In all subjects the release of lipolytic activity was higher in the deep vein, which predominantly drains muscle, than in the superficial vein, which drains mostly subcutaneous tissues such as skin and adipose tissue. This indicates that muscle is a tissue of considerable importance as a source of post heparin plasma lipolytic activity.     

Lipoprotein lipase with a defect in lipid interface recognition in a case with type I hyperlipidaemia

Defective lipoprotein lipase (LpL) was found in the postheparin plasma (PHP) of a patient with severe hypertriglyceridaemia. The patient was a 14-year-old girl with a maximum plasma triglyceride (TG) level of 3600 mg d-1 who had been suffering from recurrent pancreatitis. The patient's LpL purified from the PHP by heparin-Sepharose and phenyl-Sepharose chromatographies hydrolysed tributryrin, but not triolein emulsified with Triton X-100 and phosphatidylcholine (PC), or in chylomicrons, whereas normal LpL hydrolysed these substrates. Moreover, unlike normal LpL, LpL from the patient did not associate with VLDL, as shown by Sepharose 4B column chromatography. The patient's LpL hydrolysed triolein emulsified with lysophospholipid at a normal rate in the presence of apolipoprotein CII. These findings suggest that this patient has LpL with a normal catalytic site for tributyrin but with a defect in lipid interface recognition resulting in loss of ability to recognize VLDL or chylomicrons, but not of triolein emulsified with lysophospholipid.     

Triglyceride enrichment of HDL enhances in vivo metabolic clearance of HDL apo A-I in healthy men

Triglyceride (TG) enrichment of HDL resulting from cholesteryl ester transfer protein-mediated exchange with TG-rich lipoproteins may enhance the lipolytic transformation and subsequent metabolic clearance of HDL particles in hypertriglyceridemic states. The present study investigates the effect of TG enrichment of HDL on the clearance of HDL-associated apo A-I in humans. HDL was isolated from plasma of six normolipidemic men (mean age: 29.7 +/- 2.7 years) in the fasting state and after a five-hour intravenous infusion with a synthetic TG emulsion, Intralipid. Intralipid infusion resulted in a 2.1-fold increase in the TG content of HDL. Each tracer was then whole-labeled with 125I or 131I and injected intravenously into the subject. Apo A-I in TG-enriched HDL was cleared 26% more rapidly than apo A-I in fasting HDL. A strong correlation between the Intralipid-induced increase in the TG content of HDL and the increase in HDL apo A-I fractional catabolic rate reinforced the importance of TG enrichment of HDL in enhancing its metabolic clearance. HDL was separated further into lipoproteins containing apo A-II (LpAI:AII) and those without apo A-II (LpAI). Results revealed that the enhanced clearance of apo A-I from TG-enriched HDL could be largely attributed to differences in the clearance of LpAI but not LpAI:AII. This is, to our knowledge, the first direct demonstration in humans that TG enrichment of HDL enhances the clearance of HDL apo A-I from the circulation. This phenomenon could provide an important mechanism explaining how HDL apo A-I and HDL cholesterol are lowered in hypertriglyceridemic states.     

Catabolism of very low density lipoproteins in experimental nephrosis

The effects of experimental nephrosis in rats, produced by puromycin aminonucleoside, include an elevation of plasma levels of all lipoprotein density classes and the appearance of high density lipoprotein (HDL) rich in apoprotein (apo) A-I and deficient in apo A-IV and apo E. The hyperlipoproteinemia is associated with an increase in hepatic synthesis of lipoproteins. The possible role of decreased very low density lipoprotein (VLDL were obtained from nonfasting animals by ultracentrifugation at d 1.006 and included chylomicrons) catabolism and its relationship to the apolipoprotein composition of nephrotic high density lipoproteins (1.063 less than d less than 1.210, or 1.072 less than d less than 1.210 [HDL]) was explored. When 125I-VLDL was injected, the faster plasma clearance of lower molecular weight apolipoprotein B (apo BL) compared with that of higher molecular weight apo BH which is seen in normal rats was not observed in nephrotic rats. Less labeled phospholipid, apo C, and apo E were transferred from VLDL to higher lipoprotein density classes. Heparin-releasable plasma lipoprotein lipase and hepatic lipase activities were decreased by 50% in nephrotic rats compared with pair-fed controls. Perfusion of livers with medium that contained heparin released 50% less lipase activity in nephrotic rats than in controls. When heparin was injected intravenously, significant decreases in plasma levels of triglycerides and significant increases in levels of free fatty acids were observed in both groups of animals. In the nephrotic rats, 86% of the free fatty acids were in the lipoprotein fractions, as compared with 16% in the controls. Heparin treatment did not restore to normal the decreased apo BL clearance in nephrotic rats but it produced an increased amount of apo A-IV and apo E in the plasma HDL. In vitro addition of partially pure lipoprotein lipase to whole serum from nephrotic rats significantly increased the content of apo E in HDL. We conclude that the abnormal apoprotein composition of HDL in experimental nephrosis is the result of altered entry of apolipoproteins from triglyceride-rich lipoproteins, probably because of decreased lipolysis.     

Impaired intermediate-density lipoprotein triglyceride hydrolysis in familial lecithin: Cholesterol acyltransferase (LCAT) deficiency

A new lecithin:cholesterol acyltransferase (LCAT)-deficient family was found in Japan. In the proband, both LCAT activity and LCAT mass were deficient. The patient's parents, child, and sister, diagnosed as heterozygotes, had half-normal LCAT activity and LCAT mass. In the patient, an increase of intermediate-density lipoprotein (IDL, 1.006<d<1.019) fraction was observed. In postheparin plasma, both lipoprotein lipase and hepatic triglyceride lipase activities were low. Hydrolysis of [¹⁴C] triolein by human hepatic triglyceride lipase in patient IDL was decreased compared to that in IDL from normal postprandial serum. Preincubation of these IDL with normal plasma in the absence of 5,5′-dithiobis-(2-nitrobenzoic acid) (DTNB) increased the rate of hydrolysis, in the presence of DTNB, this increment was not observed. These results suggest that one cause of IDL increase in the LCAT-deficient patient might be the difficulty of hydrolysis of these lipoprotein particles by hepatic triglyceride lipase.     

Lipoprotein lipase in adipose tissue and plasma triglceride clearance in patients with primar hpertriglceridaemia

Abstract.

• 1 The activit of lipoprotein lipase (E.C.3.1.1.3) extracted and released from adipose tissue has been measured in obese subjects with mild or severe hpertriglceridaemia. The Intralipid® tolerance test has been studied as a measure of in vivo clearance of exogenous triglceride from plasma.
• 2 Plasma triglceride clearance was reduced in patients with severe hpertriglceridaemia (> 4 mmol/1) and this was associated with reduced activities of extracted lipoprotein lipase in adipose tissue compared to patients with mild hpertriglceridaemia (2–4 mmol/1).
• 3 A course of insulin therap (20 u/da) for 1 week increased the extracted, but not the released component of the enzme from adipose tissue of hpertri-glceridaemic patients.
• 4 Serum (25% v/v) potentiated the release of lipoprotein lipase from adipose tissue of normo- but not hpertriglceridaemic patients.
• 5 The effect of serum on enzme release was abolished if lipoprotein-deficient serum was used. Addition of ver low densit lipoprotein (VLDL) or high densit liproprotein (HDL) restored the abilit of de-lipidated serum to augment release of enzme from adipose tissue, but this was not observed with low densit lipoprotein (LDL).
• 6 It is suggested that a defect in the release of lipoprotein lipase activit in adipose tissue ma contribute to the development of hpertriglceridaemia in this group of patients.

     

毛细管等速电泳法分析肾病综合征患者的脂质代谢

目的探讨。肾病综合征（NS）患者脂蛋白组成、含量和脂质代谢酶的活性。方法用毛细管等速电泳法（cITP）将血清脂蛋白分成9种成分,结合总胆固醇（TC）浓度定量分析高密度脂蛋白胆固醇（HDL—C）和低密度脂蛋白胆固醇（LDL—C）,并根据代谢酶催化的底物／产物比值反映卵磷脂胆固醇酰基转移酶（LCAT）、脂蛋白脂肪酶（LPL）和三酰甘油酶（HL）活性。慢高密度脂蛋白（sHDL）和快高密度脂蛋白（fHDL）相对峰面积的比值可反映LCAT活性;乳糜微粒（CM）／中间密度脂蛋白（IDL）和IDL／低密度脂蛋白（LDL）比值分别反映LPL和HL活性。底物／产物比值越大,酶活性越低。结果cITP定量测定HDL—C、LDL—C与常规方法呈正相关[相关系数（r）分别为0．86、0．83,P〈0．001]。NS组sHDL／fHDL、CM／IDL、IDL／LDL比值均明显高于对照组,LCAT、LPL和HL活性均低于对照组。结论cITP可作为分析脂蛋白组成、含量和反映脂质代谢酶活性的新方法。