Biomedical subjects

J D Bagdade

Publications and source records attributed to J D Bagdade.

At least 55 records · Page 3Linked to original sources

PubMed1990

Effects of omega-3 fish oils on plasma lipids, lipoprotein composition, and postheparin lipoprotein lipase in women with IDDM.

Because the apparent reduction in cardiovascular risk noted in nondiabetic populations that ingest diets rich in marine lipids containing omega-3 fatty acids is believed to result in part from their capacity to modify the composition and physicochemical behavior of lipoproteins, we sought to determine whether dietary supplementation with marine lipids might favorably affect lipoprotein composition in insulin-dependent diabetes mellitus (IDDM). Eight normolipidemic IDDM women (mean +/- SD age 29.8 +/- 4.7 yr) were studied before and 3 mo after receiving a marine-lipid concentrate (Super-EPA) containing 6 g omega-3 fatty acids and a total of 12 mg of cholesterol daily. Weight, insulin requirements, and glycosylated hemoglobin remained stable. After treatment, mean +/- SD plasma triglyceride (TG) levels fell (before, 81.7 +/- 22 mg/dl; after, 69.19 +/- 17; P less than 0.025). High-density lipoprotein2 (HDL2) cholesterol (before, 10.98 +/- 5.45 mg/dl; after, 18.43 +/- 7.93; P less than 0.01), its major apolipoprotein A-I (apoAI), and the major phospholipids (sphingomyelin and lecithin) all rose significantly. ApoB and plasma and low-density lipoprotein cholesterol levels and HDL3 composition were unchanged. Postheparin hepatic and lipoprotein lipase activities were unaffected by marine lipids. These data indicate that women with IDDM experience apparently beneficial effects on TG and HDL2 from dietary supplementation with omega-3 fatty acids administered in a low-cholesterol-containing oil without adversely affecting overall diabetes management. If these changes in lipoprotein concentration and composition prove to have antiatherogenic consequences and are free of long-term toxicity, these agents may have a role in the therapy of IDDM patients.

Adult↗

PubMed1990

Molecular species of cholesteryl esters formed in abetalipoproteinemia: effect of apoprotein B-containing lipoproteins.

In order to study the effects of very low density (VLDL) and low density (LDL) lipoproteins on the activity and specificity of lecithin:cholesterol acyltransferase (LCAT), we determined the molecular species of cholesteryl esters (CE) synthesized in the plasma from three abetalipoproteinemic (ABL) patients, before and after supplementation with normal VLDL or LDL. The patients' plasma had significantly lower concentration of 18:2 CE and higher concentrations of 16:0 CE and 18:1 CE compared to normal plasma. Incubation of ABL plasma with [4-14C]cholesterol at 37 degrees C and the subsequent analysis of labeled CE formed by high performance liquid chromatography revealed that the major species formed was 16:0 CE (34% of total label), whereas similar incubation of the d greater than 1.063 g/ml fraction of normal plasma resulted in the formation of predominantly 18:2 CE (45% of total label). Addition of normal VLDL or LDL to ABL plasma stimulated the total LCAT activity by 30-80% and normalized the CE species synthesized. The LCAT activity of a normal d greater than 1.063 g/ml fraction also was stimulated by the normal VLDL or LDL, but there was no alteration in the species of CE formed. Most of the CE synthesized was found in the added VLDL or LDL with both ABL and normal plasma, indicating that the CE transfer (CET) activity was not affected in ABL plasma. These results suggest that while the VLDL and LDL are required for the maximal activity of LCAT, the species of CE formed are primarily determined by the molecular species composition of phosphatidylcholine in the plasma.

Abetalipoproteinemia↗

PubMed1990

Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment.

Optimally effective lipid-lowering agents should not only restore plasma lipids to normal levels but also correct potentially atherogenic alterations in lipoprotein composition and function often present in hyperlipidemic patients. Lovastatin, a competitive inhibitor of cholesterol biosynthesis, clearly lowers plasma cholesterol levels. Its effects on lipoprotein composition and cholesteryl ester transfer (CET), a key step in reverse cholesterol transport, however, are not known. Since abnormalities in CET and lipoprotein composition are present in patients with hypercholesterolemia, we studied these parameters of plasma lipoprotein transport in twelve hypercholesterolemic (HC; Type IIa) subjects (six male, six female) before and 2 months after lovastatin treatment (20 mg qd). Before lovastatin, the free cholesterol (FC)/lecithin (L) ratio in plasma, a new index of cardiovascular risk that reflects lipoprotein surface composition, was abnormally increased (1.18 +/- 0.26 vs controls 0.83 +/- 0.14; P less than 0.001) in very low density lipoproteins (VLDL) and high density lipoprotein-3 (HDL3), and remained so after treatment despite significant declines in whole plasma cholesterol (311.7 +/- 68.2 vs 215.6 +/- 27.2 mg/dl; P less than 0.001), low density lipoprotein (LDL)-cholesterol (206.3 +/- 47.9 vs 146.8 +/- 29.4; P less than 0.001), and apolipoprotein B (149 +/- 30 vs 110 +/- 17; P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effects of dietary supplementation with marine lipid concentrate on the plasma lipoprotein composition of hypercholesterolemic patients.

Although the triglyceride-lowering actions of n-3 fatty acids of marine lipids are now well-recognized, their effects on plasma lipoproteins have not been studied systematically in patients with hypercholesterolemia. To address this question, we supplemented the Phase 1 American Heart Association diets of 14 hypercholesterolemic ambulatory outpatients with a commercially available preparation of marine lipid concentrate (SuperEPA) containing 7.5 g n-3 fatty acids per day and studied their plasma lipids and lipoproteins before and after 30 days of treatment. Both plasma triglyceride and cholesterol levels fell uniformly in all patients while the mean VLDL- and LDL-cholesterol decreased by 58% (P less than 0.005) and 13% (P less than 0.025) respectively. The decrease in whole plasma cholesterol was significantly correlated with the fall in LDL-cholesterol (r = 0.85, P less than 0.01), and not VLDL-cholesterol (r = 0.39, NS). Among the other potentially beneficial actions observed was an increase in HDL2 in all patients (mean increment 41%, P less than 0.005), and an increase in the HDL2/HDL3 ratio (+46%, P less than 0.001) and decreases in the LDL/HDL ratio (-14%, P less than 0.005) and in the unesterified cholesterol/lecithin ratio (-17%; P less than 0.001) in plasma. The increase in the unesterified cholesterol/esterified cholesterol ratio in VLDL and HDL3 suggested that marine lipid therapy resulted in a reduction in the size of lipoprotein particles in these fractions. Since these changes may reduce cardiovascular risk, these findings suggest that marine lipids may prove useful in the treatment of certain patients with hypercholesterolemia.

Adult↗

PubMed1989

Whole-plasma and high-density lipoprotein subfraction surface lipid composition in IDDM men.

To determine whether compositional abnormalities are present in high-density lipoprotein (HDL) in patients with insulin-dependent diabetes mellitus (IDDM) that might negate its putatively protective cardiovascular effects, we studied the plasma lipoproteins of 12 men with varying degrees of clinical control (mean fasting glucose 193 +/- 10 mg/dl, mean glycoalbumin greater than 73% above control mean). The diabetic patients' basal plasma triglyceride, total- and free- (unesterified) cholesterol, HDL cholesterol (HDL-chol), and apolipoprotein AI, AII, and B concentrations were similar to those of control subjects, but the free-cholesterol-to-lecithin ratio, a new index of cardiovascular disease risk, was significantly increased in their plasma (0.97 +/- 0.14 vs. 0.88 +/- 0.07, P less than .02) and their very-low-density lipoprotein (VLDL)-low-density lipoprotein (LDL) subfraction (1.50 +/- 0.51 vs. 1.08 +/- 0.15, P less than .005). Although HDL2-chol was similar in diabetic and control groups, the HDL2-chol-to-free-cholesterol ratio (diabetic vs. control, 4.64 +/- 1.7 vs. 1.96 +/- 1.0 mumol/ml, P less than .025) and the sphingomyelin-to-lecithin ratio (0.23 +/- 0.08 vs. 0.20 +/- 0.09, P less than .025) were both significantly increased in the IDDM group. HDL3-chol was higher in the IDDM than in the control subjects (diabetic vs. control, 38.6 +/- 5.2 vs. 32.7 +/- 2.7 mg/dl, P less than .005). In contrast to whole plasma and the VLDL + LDL subfraction, the free-cholesterol-to-lecithin ratio of IDDM and control HDL subfractions were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Molecular species of phosphatidylcholine in abetalipoproteinemia: effect of lecithin:cholesterol acyltransferase and lysolecithin acyltransferase.

In order to study the role of very low density lipoproteins (VLDL) and low density lipoproteins (LDL) in determining the molecular species composition of phosphatidylcholine (PC) and the specificity of lecithin:cholesterol acyltransferase (LCAT) in human plasma, we studied the PC species composition in plasma from abetalipoproteinemic (ABL) and control subjects before and after incubation at 37 degrees C. The ABL plasma contained significantly higher percentages of sn-2-18:1 species (16:0-18:1, 18:0-18:1, and 18:1-18:1) and lower percentages of sn-2-18:2 species (16:0-18:2, 18:0-18:2, and 18:1-18:2) as well as sn-2-20:4 species (16:0-20:4, 18:0-20:4, and 18:1-20:4). Similar abnormalities were found in the PC of ABL erythrocytes, while the PE of the erythrocytes was less affected. The relative contribution of various PC species towards LCAT reaction in ABL plasma was significantly different from that found in normal plasma. Thus, while 16:0-18:2 and 16:0-18:1 contributed, respectively, 43.8% and 15.9% of the total acyl groups used for cholesterol esterification in normal plasma, they contributed, respectively, 21.5% and 37.9% in ABL plasma. The relative contribution of 16:0-20:4 was also significantly lower in ABL plasma (4.7% vs. 9.0% in normal), while that of 16:0-16:0 was higher (6.4% vs. 0.5%). However, the selectivity factors of various species (percent contribution/percent concentration) were not significantly different between ABL and normal plasma, indicating that the substrate specificity of LCAT is not altered in the absence of VLDL and LDL. Incubation of ABL plasma in the presence of normal VLDL or LDL resulted in normalization of its molecular species composition and in the stimulation of its LCAT activity. Addition of LDL, but not VLDL, also resulted in the activation of lysolecithin acyltransferase (LAT) activity. The incorporation of [1-14C]palmitoyl lysoPC into various PC species in the presence of LDL was similar to that observed in normal plasma, with the 16:0-16:0 species having the highest specific activity. These results indicate that the absence of apoB-containing lipoproteins significantly affects the molecular species composition of plasma PC as well as its metabolism by LCAT and LAT reactions.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1989

Abnormal high-density lipoprotein composition in women with insulin-dependent diabetes.

To determine whether alterations in lipoprotein phospholipid composition might be an unrecognized factor that contributes to the unexplained acceleration of atherogenesis and the loss of sex-related protection from the development of coronary heart disease in women with insulin-dependent diabetes mellitus, we have estimated levels of neutral lipids, apolipoproteins (A-I, A-II, B), and free cholesterol (FC) in plasma and the four major phospholipid constituents of the very low-density lipoprotein + low-density lipoprotein and high-density lipoprotein (HDL) fractions in 12 ambulatory female patients with varying degrees of diabetic control. Although levels of triglyceride, cholesterol, HDL-cholesterol, and lipoprotein phospholipids in whole plasma of the patients with diabetes were similar to those in controls, their FC levels and FC/lecithin ratio, a recently described index of cardiovascular risk, both were abnormally increased (p less than 0.01). In the HDL-containing plasma fraction, concentrations of sphingomyelin, lecithin, and lysolecithin all were significantly reduced (p less than 0.05; p less than 0.01, and p less than 0.02, respectively). These compositional changes may be potentially atherogenic, because a reduction in the phospholipid content of HDL may impair its capacity to promote the efflux of cholesterol from cells, and the transfer of cholesterol ester from HDL to the larger apo-B-containing lipoproteins is inhibited when their content of FC is increased relative to phospholipid. These previously unrecognized qualitative defects, which are inapparent in the routine estimation of plasma lipids, may compromise reverse cholesterol transport and thereby promote atherogenesis in women with insulin-dependent diabetes mellitus.

Adult↗

PubMed1988

Influence of low estrogen-containing oral contraceptives on lipoprotein phospholipid composition and mononuclear cell membrane fluidity.

Since the effects of the new low estrogen-containing oral contraceptive (OC) preparations on lipoprotein phospholipid (PL) composition are unknown, we studied 3 groups of 10 young women before and after 6 months of use of 3 commonly prescribed agents containing almost identical amounts of ethinyl estradiol (0.30-0.35 microgram) and differing progestogens, and correlated these changes with their estrogen to progestin (E/P) ratio. The directional changes in both plasma neutral lipid and PL concentrations tended to correlate with the E/P ratio, with plasma HDL-cholesterol (HDL-C) falling slightly and the low density lipoprotein-cholesterol (LDL-C)/HDL-C ratio increasing in the women taking the OC with the lowest E/P ratio; in contrast, plasma HDL-C increased and the LDL-C/HDL-C ratio fell in those receiving the preparation with the highest E/P ratio. In HDL, the ratio of the 2 principal PL, sphingomyelin and lecithin, an index of lipid fluidity, tended to increase, suggesting that the surface of this lipoprotein class had become more rigid. This change was most apparent in women receiving the agent in which the progestin was predominant; in women receiving the preparations with the higher E/P ratios the sphingomyelin/lecithin ratio actually declined. The membrane fluidity of mononuclear cells obtained from five women taking an OC with a relatively high E/P ratio, however, was significantly increased (P less than 0.007) compared to that in normal women. These findings demonstrate that, even with substantial reductions in their estrogen content, the use of these newer OC is associated with quantitative and qualitative changes in lipoprotein PL composition that parallel their E/P balance and are associated with altered fluidity of mononuclear cell membranes.

Adolescent↗

PubMed1987

Effects of serum from oral contraceptive users on the metabolism of low density lipoprotein.

The metabolism of radiolabeled 125I-low density lipoprotein (LDL) was studied in cultured human aortic smooth muscle cells (SMC) to investigate potential mechanisms contributing to heart attack and stroke in young women taking oral contraceptive (OC) preparations. No consistent difference was discerned in the capacity of these cells to bind and internalize LDL following 24-hour exposure to pooled lipoprotein-poor (d greater than 1.25 gm/ml) serum from nonsmoking OC users and controls. However, significantly (p greater than 0.01) less soluble radioactive material was released into the media from dishes containing SMC incubated with OC serum, indicating that their capacity to degrade LDL was impaired. Increased amounts of both cholesterol and cholesterol ester and electron microscopic evidence of lipid accumulation were found in SMC grown for 12 days under standard culture conditions with 10% OC serum. This combination of in vitro findings suggests that OC use may accelerate the development of cardiovascular disease in some women by modifying the metabolism of LDL by cells of the arterial wall.

Adolescent↗

PubMed1986

Endocrine emergencies.

Endocrine emergencies are relatively infrequent events in clinical practice. Correct management requires prompt recognition and treatment, frequent without supporting laboratory studies. An understanding of the pathophysiology of these acute states of hormone excess or deficiency assists in establishing the correct diagnosis and initiating the proper therapy.

Adrenal Cortex Diseases↗

PubMed1986

Glucocorticoid-related impairment in the metabolism of low density lipoprotein by human fibroblasts.

The metabolism of radiolabelled 125I-low density lipoprotein (LDL) was studied in cultured human dermal fibroblasts to investigate potential mechanisms contributing to the accelerated development of cardiovascular disease in patients treated chronically with corticosteroids. Fibroblasts exposed for 48 hours to pooled lipoprotein-poor (d greater than 1.25 gm/ml) serum from glucocorticoid-treated patients showed an increased capacity to bind LDL (p less than .001) compared to cells incubated under identical conditions with pooled serum from controls. In addition, a significantly (p less than .001) reduced amount of soluble radioactive material appeared in the media indicating that exposure of fibroblasts to corticosteroid serum also impaired their capacity to degrade LDL. If this tendency of cultured cells to accumulate cholesterol-rich lipoprotein when exposed to constituents of serum from these patients is present in patients receiving long-term treatment with glucocorticoids, it might influence arterial lipid accumulation and accelerate their developing cardiovascular disease.

Adolescent↗

PubMed1985

Substrate specificity of plasma lysolecithin acyltransferase and the molecular species of lecithin formed by the reaction.

Human plasma lecithin-cholesterol acyltransferase also converts lysolecithin to lecithin in the presence of low density lipoproteins. To understand the physiological importance of this lysolecithin acyltransferase reaction, we investigated the molecular species of lysolecithin available for acylation in normal plasma and the lecithins which are formed by the acylation of each of these lysolecithins. Palmitate- and stearate-containing lysolecithins were formed by the lecithin-cholesterol acyltransferase reaction, whereas oleate- and linoleate-containing lysolecithins were formed by the action of post-heparin lipase(s). All the natural lysolecithins were esterified at comparable rates by the isolated enzyme. Lyso platelet-activating factor was esterified about 70% as efficiently as the lysolecithins, while lysophosphatidylethanolamine was esterified at about 30% the rate observed with lysolecithin. The 2-acyl isomers of lysolecithin were acylated to the same extent as the 1-acyl isomers, although considerable isomerization of the former took place during the incubation. There were no net changes in the concentrations of lecithin and lysolecithin after 6 h of incubation with the enzyme, although over 10% of the labeled lysolecithin was converted to lecithin, indicating that the endogenous lecithin serves as the acyl donor in the reaction. When the molecular species of lecithin formed were analyzed by high performance liquid chromatography, the same pattern of fatty acid incorporation was observed with all the lysolecithins used. The bulk of the radioactivity was incorporated into molecular species formed by the acylation with linoleic, oleic, and palmitic acids, in decreasing order. However, in each case, the lecithins formed by acylation with palmitic acid had the highest specific radioactivity, followed by those acylated with linoleic and oleic acids. From these results it is postulated that the enzyme alters the molecular species composition of lecithin in plasma without increasing the net amount of total lecithins.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1985

The measurement of arterial smooth muscle cell mitogens in the blood of oral contraceptive users.

We have previously shown that serum from young women receiving the same combined mestranol-norethindrone containing oral contraceptive (OC) preparation accelerated the proliferation of arterial smooth muscle cells (SMC) in tissue culture, and this in vitro effect was not a direct action of either of its estrogenic or progestogenic constituents. To identify the substance(s) which might contribute to this potentially atherogenic action, blood was obtained from 20 OC users and control women for the measurement of growth hormone, insulin, somatomedins (insulin-like growth factor IGF-I and IGF-II), and the platelet alpha-granule constituents platelet-derived growth factor (PDGF), beta-thromboglobulin, and platelet factor 4 (PF4). No difference was demonstrable between OC users and controls in the levels of any of these growth-promoting hormones, nor in plasma concentrations of any of the platelet alpha-granule proteins. These studies indicate that the enhanced mitogenicity found in OC sera is probably not attributable directly to these hormones or PDGF, and may instead result from an in vivo OC-induced alteration in other as yet unidentified mediators of cellular growth.

Adolescent↗

PubMed1985

Role of low density lipoprotein in the activation of plasma lysolecithin acyltransferase activity. Effect of chemical and enzymatic modifications of the lipoprotein on enzyme activity.

The effect of various chemical and enzymatic modifications of low density lipoprotein (LDL) on its ability to activate the isolated human plasma lysolecithin acyltransferase (LAT) was studied. Removal of all lipids from LDL resulted in the complete loss of LAT activation. Removal of only neutral lipids by extraction with heptane retained up to 50% of the original activity, which was not increased further by reconstitution of the LDL with the extracted lipids. Hydrolysis of the diacylphosphoglycerides of the LDL with phospholipases resulted in complete loss of LAT activation which was partially restored by the addition of egg lecithin. Hydrolysis of more than 4% of LDL protein by trypsin led to a linear decrease in activity with complete loss of activity occurring when about 25% of the LDL protein is hydrolyzed. Modification of the arginine groups of LDL reversibly inhibited the activation of LAT. Modification of lysine residues of LDL by acetylation, acetoacetylation or succinylation also abolished its ability to activate lysolecithin acylation.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1982

Polyamines and atherosclerosis. Platelet releasate and other mitogens stimulate putrescine transport in arterial smooth muscle cells.

Although polyamine (PA) levels are believed to increase in response to mitogenic stimuli in all cells during growth, their role in arterial smooth muscle cell (ASMC) proliferation, an essential step in atherogenesis, is unknown. To determine whether the arterial wall mitogen, platelet-derived growth factor (PDGF) influences PA metabolism when cell cycle traverse is initiated, we examined its effects on the transport of the PA precursor [3H]putrescine (PUT) in culture in bovine and human ASMC. PUT uptake was stimulated in a dose-response relationship by PDGF-containing human serum (2-10%), and abolished in 24 h without it. Inhibition of this uptake by spermidine and the lack of effect of thymidine, leucine and ornithine indicated that uptake was by a PA-specific mechanism. Without serum, platelet releasate containing PDGF stimulated PUT uptake but not that of leucine or glucose. While platelet-poor plasma alone also promoted PUT uptake, the combination of platelet releasate and platelet-poor plasma was required for maximal DNA synthesis. PUT uptake under these conditions reached a peak at 16 h, while the synthesis of DNA was maximal at 24 h. Supraphysiological concentrations of insulin, and fibroblast and epidermal growth factors, also stimulated the uptake of the labeled PUT both in the absence and presence of serum, but at much lower rates than those observed with platelet releasate. These findings indicate that the early replicative actions of a variety of mitogens for ASMC involve stimulation of PUT uptake and suggest that PA uptake must precede the initiation of DNA synthesis in ASMC during atherogenesis.

Arteries↗

PubMed1982

Studies on the cofactor requirement for the acylation and hydrolysis reactions catalyzed by purified lecithin-cholesterol acyltransferase. Effect of low density lipoproteins and apolipoprotein A-i.

Because lecithin-cholesterol acyltransferase (LCAT) has been shown to carry out acylation of lysolecithin as well as hydrolysis of lecithin in addition to an esterification of cholesterol, the cofactor requirements of the three reactions catalyzed by the enzyme were studied. The purified enzyme required apolipoprotein A-I (apo A-I) for both the phospholipase A2 activity (release of free fatty acids from lecithin) and cholesterol esterification, whereas, low density lipoprotein (LDL) was required for the acylation of lysolecithin. Apo A-I and lecithin liposomes could not substitute for LDL for the activation of lysolecithin acyltransferase activity. Removal of apo A-I from the LDL preparation by affinity chromatography did not affect the activation of lysolecithin acylation, indicating that the contaminating apo A-I is not responsible for the activation. LDL facilitates cholesterol esterification in presence of labelled lecithin liposomes by providing the unesterified cholesterol. Removal of contaminating apo A-I, however, abolishes this LCAT activity which could be restored by addition of pure apo A-I. Lysolecithin inhibits both phospholipase A2 and LCAT activities, but LDL appeared to attenuate the effects of lysolecithin, in addition to stimulating the acylation of lysolecithin. These results show that apo A-I is not obligatory for all the reactions carried out by the enzyme, and that LDL plays an important role in the regulation of the hydrolysis and acylation reaction carried out by the enzyme.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1982

Host defense mellitus: defective membrane synthesis during phagocytosis.

During phagocytosis, polymorphonuclear leukocytes from poorly controlled diabetic patients convert lysolecithin to lecithin at a lower rate than cells from control subjects. This defect is partially reversed by treatment with insulin. By reducing the availability of structural lipid for formation of the phagocytic vacuole which normally takes place during phagocytosis, this impairment may compromise cellular host-defense mechanisms in some diabetic patients.

Adult↗

PubMed1982

Lecithin: cholesterol acyltransferase activity in dialyzed and undialyzed chronic uremic patients.

Lecithin cholesterol acyltransferase (LCAT) and lysolecithin acyltransferase (LAT) activities in plasma were significantly lower in undialyzed than in dialyzed uremic patients and controls. Both LCAT and LAT activities were normal in the maintenance dialysis group. The free/total cholesterol ratio was significantly increased in the undialyzed patients only. This ratio and LCAT were inversely related in the dialyzed group, unrelated in the undialyzed patients, and positively correlated in controls. Unlike non-uremic populations with hypertriglyceridemia in which LCAT is increased, no correlation was found between plasma triglyceride and LCAT in the uremic population studied. Our results show that both LCAT and LAT activities are reduced in undialyzed chronic uremic patients but are not significantly different from control levels in patients treated with chronic hemodialysis. These results indicate that the changes in LCAT activity contrast with those described in lipoprotein composition and metabolism which do not appear to be affected by chronic dialysis therapy.

1-Acylglycerophosphocholine O-Acyltransferase↗