| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol ester in corpus luteum of rat observed by analytical color fluorescence electron microscopy Ning, G., T. Fujimoto, et al. (1993), J Histochem Cytochem 41(4): 617-25. Abstract: We used an analytical color fluorescence electron microscope to observe cathodoluminescence (CL) in the corpus luteum of rat. CL was emitted from lipid droplets and has a typical spectrum of two peaks at wavelengths of 320 and 430 nm. The intensity of CL at 320 nm (CL320) in the corpus luteum showed a regular change during an estrous cycle: it was very weak at the newly formed stage, gradually increased, reached the maximum at diestrus 2, and then began to diminish at proestrus except in the patches of degenerated cells. CL320 decreased during early stages of pregnancy or after prolonged treatment with 4-aminopyrazolo-pyrimidine; CL at 430 nm (CL430) remained clearly visible. CL320 showed a strong emission from degenerated luteal cells 10 days after hypophysectomy, but was diminished in cells rescued by injection of 50 IU pregnant mare's serum gonadotropin. In the luteal cells of luteinized ovary 2 hr after intravenous injection of 10 IU luteinizing hormone, CL was barely detected. CL320 in interstitial cells was also weak in the rats hypophysectomized and then treated with pregnant mare's serum gonadotropin, and in the 4-aminopyrazolo-pyrimidine-treated rats, although it has little change through a natural estrous cycle. The results are consistent with the assumption that the content of cholesterol ester is reflected by the intensity of CL320 emitted from the lipid droplets of rat luteal cells. The possibility was shown that the condition of steroidogenesis can be monitored through CL analysis by microscopy. |
| Cholesterol ester storage disease in two siblings Perez Rodriguez-Cuesta, J. M., J. I. Suarez Tomas, et al. (1990), An Esp Pediatr 32(3): 249-52. Abstract: Two children, male y and female brothers, with a cholesterol ester storage disease are presented. Some pathogenic, clinical biochemical and histopathological aspects are commented. The ultrastructural hepatic finding of microcrystallized cholesterol in the Von Kupffer's cells was the determinant diagnostic parameter in both cases. The clinical expression and evolution was different, with a biggest functional impairement in the male, which was submitted to hepatic transplantation. |
| Cholesterol ester transfer and high-density lipoprotein conversion in normolipidemic, hypercholesterolemic, and hypertriglyceridemic non-insulin-dependent diabetics Pulcini, T., M. Elchebly, et al. (1995), Biochem Mol Med 55(1): 54-60. Abstract: Non-insulin-dependent diabetes (NIDD) is a situation at elevated risk for atherosclerosis. The plasma concentration of high-density lipoprotein (HDL) is often lowered. This may be accompanied by an abnormal composition and profile of HDL subfractions. These abnormalities might result in part from a defect in the net cholesterol ester transfer (CET) from HDL to apo B-containing lipoproteins. In the present work, we have studied the net CET and HDL conversion in normolipidemic, hypercholesterolemic, and hypertriglyceridemic NIDD, by comparison with control subjects. HDL conversion was determined by gradient gel electrophoresis after 23 h incubation in plasma with HDL3 labeled with a nontransferable synthetic marker. The net CET in normolipidemic NIDD was similar to that of controls, while it was approximately doubled in hypercholesterolemic or hypertriglyceridemic NIDD. In all groups, HDL conversion was comparable, with the exception of hypertriglyceridemic NIDD. In the latter group, the labeled HDL2/HDL3 ratio was increased, indicating a more complete conversion that was correlated with the triglyceride/cholesterol ester ratio in HDL. In addition, when lecithin:cholesterol acyl transferase was inhibited, a distinct peak of small HDL particles appeared in the density range of HDL2 in contrast with the other groups where only small HDL3 was formed. Recombination experiments showed that these abnormalities were attributable to the plasma in which labeled HDL3 was incubated rather than to the origin (control or hypertriglyceridemic NIDD) of labeled HDL3. These data suggest that in NIDD, hypertriglyceridemia may result in abnormalities of HDL conversion due to alterations in HDL composition.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol ester transfer mediated by lipid transfer protein as influenced by changes in the charge characteristics of plasma lipoproteins Nishida, H. I., H. Arai, et al. (1993), J Biol Chem 268(22): 16352-60. Abstract: The relationship between the cholesterol ester (CE) transfer activity of lipid transfer protein (LTP) and its affinity with lipid and lipoprotein particles was investigated. The study of the effects of chemical modification of low density lipoprotein (LDL) amino groups and carboxyl groups on the CE transfer activity showed that the maximal activity is obtained upon succinylation or acetylation of approximately 7% of LDL amino groups. Further increases in the extent of modification progressively reduced the transfer activity. The treatment of LDL with fatty acids gave results comparable to the chemical modification of LDL amino groups. The addition of low concentrations of fatty acids was stimulatory, while that of high concentrations was inhibitory. Although increases in the positive charges of LDL by the carboxyl group modification did not appreciably influence the CE transfer, the addition of cationic detergents gave a profound effect on the CE transfer. A maximal CE transfer activity was obtained upon addition of very small amounts of the detergents, with the higher concentrations sharply reducing the transfer activity. We also studied the effects of the concentrations of phosphate buffer and various salts on the CE transfer as well as the affinity of LTP for very low density lipoproteins, low density lipoproteins, high density lipoproteins 3, and high density lipoproteins 2. It appeared that the affinity of LTP for various lipoproteins is governed by a delicate balance of electrostatic and hydrophobic interactions. Optimal degrees of the interaction of LTP with both donor and acceptor particles seem to be required for the maximal degree of CE transfer. |
| Cholesterol ester transfer protein (CETP) Bujo, H. and Y. Saito (1990), Nippon Rinsho 48(11): 2492-7. |
| Cholesterol ester transfer protein (CETP) Nakaya, N. (1994), Nippon Rinsho 52(12): 3164-9. Abstract: Plasma CETP plays an important role in the reverse cholesterol transport system in conjunction with lecithin:cholesterol acyltransferase (LCAT). CETP mediates transfer of cholesteryl ester from HDL to apo B containing lipoproteins and also mediates transfer of triglyceride from VLDL and IDL to HDL. In this review, molecular characteristics, mechanism of lipid transfer, site of synthesis, factors regulating production and activity of CETP and lipoprotein abnormalities in CETP deficiency were described. High activity of CETP is considered to promote atherosclerosis, because the lipoprotein changes resulting from CETP activity are completely atherogenic and animals who have low CETP activity are resistant to atherosclerosis. |
| Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease in the Turkish population Isbir, T., H. Yilmaz, et al. (2003), Clin Genet 64(3): 228-34. Abstract: The aim of this study was to compare patients with coronary artery disease (CAD) to healthy objects, in order to explore a possible association between CAD and the variants in the gene encoding cholesterol ester transfer protein (CETP), apolipoprotein E (Apo E) and lipoprotein lipase (LPL). The relationship between CETP MspI, apo E and LPL PvuII gene polymorphisms and serum lipids were investigated in 173 patients with CAD and 111 healthy controls. The frequency of Apo epsilon4 (p < 0.05) and CETP M1 (p < 0.01) alleles were higher in the CAD group than in the control group. In the CAD group, those with the Msp M1 allele had higher levels of total cholesterol (TC) (p = 0026) and low-density lipoprotein cholesterol (LDL-C) than those with the Msp M2 allele. Subjects with an epsilon2 allele had the lowest levels of TC and LDL-C, while subjects with the epsilon4 allele had the highest. In the control group, CETP, the Msp M2 allele was associated with a higher level of high-density lipoprotein cholesterol (HDL-C) (p = 0.012) than the Msp M1 allele. The distributions of LPL genotype and allele did not differ between the CAD and control groups. The present study demonstrates that the CETP Msp1 and Apo E gene polymorphisms are associated with variations in lipids in patients with CAD and healthy controls in Turkish population. |
| Cholesterol ester transfer protein. A major player in cholesterol metabolism Hansen, P. R. (1999), Ugeskr Laeger 161(38): 5295-8. Abstract: Plasma cholesterol transfer protein (P-CETP) plays a central role in cholesterol metabolism by pronroting transfer of cholesteryl esters from high density lipoprotein (HDL) to very low density lipoproteins in exchange for triglycerides. The CETP-reaction may hereby be a critical factor in reverse cholesterol transport, i.e., the transfer of cholesterol from peripheral tissues to the river for catabolism. Human genetic CETP deficiency is associated with increased P-HDL-cholesterol, whereas CEPT transgenic mice display decreased P-HDL-cholesterol. The effects of CETP on atherogenesis are currently unpredictable, and they are likely to depend on the metabolic context. However, the presence of specific polymorphisms in the CETP gene may be of clinical importance, and CETP should be considered among the factors relevant for differentiation of dyslipidemic syndromes associated with susceptibility to and protection from atherosclerotic disease. |
| Cholesterol ester transfer protein: a molecule with three faces? Stevenson, C. G. (1998), Crit Rev Clin Lab Sci 35(6): 517-46. Abstract: The pathogenesis of atherosclerosis continues to be a focus of intensive study. One of the more recent players in the atherosclerosis drama is cholesterol ester transfer protein (CETP). CETP is primarily involved in lipid transfer between lipoproteins, for example, from high-density lipoproteins (HDL) to apo B-containing lipoproteins, but CETP has also been found to take up cholesterol directly from cells without the co-participation of lipoproteins, and it is still not clear whether CETP should be classified as a beneficial or as a harmful protein. Some of the important evidence for these conflicting theories is examined here, with special reference to situations where CETP appears to be proatherogenic, instances where CETP seems to assume an antiatherogenic role, and situations where CETP seems to be both proatherogenic and antiatherogenic. In addition, the metabolic context of CETP and the modification of CETP substrates play crucial roles that are not always recognized when judgements about the role of CETP in atherosclerosis are recorded. |
| Cholesterol esterase accelerates intestinal cholesterol absorption Ikeda, I., R. Matsuoka, et al. (2002), Biochim Biophys Acta 1571(1): 34-44. Abstract: Mechanisms of acceleration of cholesterol absorption by cholesterol esterase were investigated in various experimental conditions. Lymphatic recovery of cholesterol intubated as a micellar solution containing phosphatidylcholine (PC) into the duodenum was enhanced by the co-administration of cholesterol esterase in rats drained of bile and pancreatic juice. However, no accelerated incorporation was observed when cholesterol was solubilized in PC-depleted micelles. Cholesterol esterase dose-dependently accelerated the incorporation of cholesterol into differentiated Caco-2 cells, only when cholesterol was solubilized in PC-containing micelles. The accelerated incorporation of cholesterol into Caco-2 cells by cholesterol esterase disappeared when the enzyme was preincubated with a suicide inhibitor of cholesterol esterase. Cholesterol esterase has an activity as phospholipase A(2). When 10% of PC in bile salt micelles was replaced by lysophosphatidylcholine (lysoPC), the incorporation of cholesterol into Caco-2 cells was significantly accelerated. Cholesterol esterase enhanced the incorporation of micellar cholesterol into brush border membranes prepared from the rat jejunum. The addition of cholesterol esterase to bile salt micelles accelerated the release of micellar cholesterol in a dose-dependent manner, only when the micelles contained PC. These observations strongly suggest that cholesterol esterase hydrolyzes PC in bile salt micelles and thereby, accelerating the release of cholesterol from bile salt micelles. This may be a major cause of the acceleration of cholesterol absorption by cholesterol esterase. |
| Cholesterol esterase and cholesterol oxidase immobilized onto arylamine glass beads Malik, V., S. Singh, et al. (2002), Sheng Wu Gong Cheng Xue Bao 18(2): 155-61. Abstract: Cholesterol esterase (CEase) from bovine pancreas and cholesterol oxidase (COD) from Bravibacterium recombinant type have been immobilized individually and co-immobilized onto arylamine glass (pore diameter 55 nm) through the process of diazotization. CEase and COD retained 92.65% and 85.54% of the initial activity with conjugation yields of 7.2 mg/g and 8.3 mg/g support respectively when immobilized individually on arylamine glass beads, but retained 89.58% of the initial activity with a conjugation yield of 2.9 mg/g support when co-immobilized on the same support. The effects of pH, temperature, time of incubation, substrate concentration, serum inorganic salts & metabolites, thermal stability, storage stability in cold and reusability on the immobilized enzymes were studied and compared with those of free enzymes. The analytic use of both individually immobilized and co-immobilized enzymes in discrete analysis of total and free cholesterol in serum is demonstrated. |
| Cholesterol esterase bound to intestinal brush border membranes does not accelerate incorporation of micellar cholesterol into absorptive cells Ikeda, I., K. Mitsui, et al. (2003), Biosci Biotechnol Biochem 67(11): 2381-7. Abstract: We confirmed that cholesterol esterase accelerated the incorporation of unesterified cholesterol solubilized in bile salt micelles into differentiated Caco-2 cells under various experimental conditions. Rat pancreatic juice and bovine cholesterol esterase increased the incorporation of micellar cholesterol into rat intestinal brush border membranes. The incorporation of micellar cholesterol was not changed in the brush border membranes enriched in and depleted of cholesterol esterase. The results suggest that the accelerated incorporation of micellar cholesterol by cholesterol esterase into absorptive cells is not mediated by the enzyme bound to the brush border membranes. |
| Cholesterol esterase in preglomerular microvessels from normal and cholesterol-fed rabbits Kamanna, V. S., S. I. Saied, et al. (1991), Am J Physiol 261(1 Pt 2): F163-8. Abstract: Feeding cholesterol to rabbits produces an atherosclerotic model sharing common metabolic features with the disease in humans, including the vascular lipid accumulation. In coronary vascular cells, this lipid accumulation has been associated with decreased prostacyclin (PGI2) biosynthesis and acid cholesterol esterase activity. Unlike the coronary vascular bed, renal microvasculature appears relatively resistant to atherosclerotic injury. This study examined whether renal microvessels from cholesterol-fed rabbits demonstrated similar metabolic changes in coronary vascular cells. Rabbits were fed either a 0% or 2% cholesterol diet for 1 mo. Similar to coronary vascular cells, in renal microvessels from cholesterol-fed rabbits PGI2 biosynthesis decreased and tissue concentrations of cholesterol and cholesteryl esters increased. However, unlike coronary vascular cells, renal microvascular cholesterol esterase activity increased. Light and electron microscopy revealed sporadic lipid deposits in renal microvessels from cholesterol-fed rabbits and no foam cells or occlusive lesions. In vitro addition of prostanoids to normal renal microvessels had no effect on cholesterol esterase activity. It is inviting to speculate that the increased acid cholesterol esterase activity in renal microvessels from cholesterol-fed rabbits protected them from developing extensive microvascular lesions. These biochemical events may explain the relative resistance of human renal microvessels to the development of occlusive atherosclerotic microvascular lesions. |
| Cholesterol esterification and Niemann-Pick disease: an approach to identifying the defect in fibroblasts Bowler, L. M., R. Shankaran, et al. (1990), J Neurosci Res 27(4): 505-11. Abstract: Fibroblasts from 13 patients with the clinical phenotype of type IIS, Niemann-Pick disease were evaluated for their ability to incorporate oleic acid into cholesterol esters via an LDL responsive mechanism. Eight patients displayed a severe deficiency (less than 8% of normal) of cholesterol ester (CE) synthesis while a clinically less affected group displayed intermediate levels (36% of normal) of synthetic capacity with no detectable overlap between these groups and the control range. There was no deficiency in cholesterol ester production in fibroblasts from a patient with Zellweger's disease, a disorder characterized by altered peroxisomes and abnormal peroxisomal cholesterol metabolism, while in I-cell disease, characterized by a primary deficiency of a phosphotransferase which results in altered targeting of lysosomal hydrolases, it was reduced to 25% of the control level. To further implicate lysosomal proteins in the etiology of type IIS, Niemann-Pick disease we measured the effect of correction (conditioned) medium, and the lysosomotropic agent, NH4Cl on cholesterol ester synthesis in fibroblasts. NH4Cl completely inhibited incorporation into CE by normal cells, thus mimicking the CE defect in type IIS, Niemann-Pick cells. Conditioned medium had no effect on incorporation into CE synthesis but medium conditioned in the presence of 10 mM NH4Cl stimulated incorporation into CE in the control but not in Niemann-Pick cells. When Niemann-Pick cells cultured in the presence of NH4Cl were challenged to synthesize CE in the absence of NH4Cl, a significant enhancement of CE synthesis was noted in representative cell lines from both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol esterification by host and parasite is essential for optimal proliferation of Toxoplasma gondii Sonda, S., L. M. Ting, et al. (2001), J Biol Chem 276(37): 34434-40. Abstract: Upon host cell invasion the apicomplexan parasite Toxoplasma gondii resides in a specialized compartment termed the parasitophorous vacuole that is derived from the host cell membrane but modified by the parasite. Despite the segregation of the parasitophorous vacuole from the host endocytic network, the intravacuolar parasite has been shown to acquire cholesterol from the host cell. In order to characterize further the role of sterol metabolism in T. gondii biology, we focused our studies on the activity of acyl-CoA:cholesterol acyltransferase (ACAT), a key enzyme for maintaining the intracellular homeostasis of cholesterol through the formation of cholesterol esters. In this study, we demonstrate that ACAT and cholesterol esters play a crucial role in the optimal replication of T. gondii. Moreover, we identified ACAT activity in T. gondii that can be modulated by pharmacological ACAT inhibitors with a consequent detrimental effect on parasite replication. |
| Cholesterol esterification in human monocyte-derived macrophages is inhibited by protein kinase C with dual roles for mitogen activated protein kinases Napolitano, M., M. Avella, et al. (2004), Cell Biol Int 28(10): 717-25. Abstract: The possible role of protein kinase C (PKC) and mitogen activated protein (MAP) kinases in the stimulation of cholesterol esterification by acetylated low density lipoprotein (acLDL) in human monocyte-derived macrophages (HMDM) was studied. Cholesterol esterification, as assessed by the rate of incorporation of 3H-oleate into cholesteryl ester, was markedly higher in HMDM incubated with acLDL as compared to native LDL (nLDL). In the presence of the phorbol ester, phorbol 12-myristate 13-acetate (PMA, 100 nM), however, the rate of incorporation was reduced by about 50% and 85% in incubations with nLDL and acLDL, respectively. Thus, the difference in the rate of cholesteryl esterification induced by the two types of lipoprotein was abolished by PMA, indicating that PKC activation inhibits the process, and this was confirmed by the finding that the PKC inhibitor calphostin C reversed the PMA-induced inhibition of cholesterol esterification. Incubation of HMDM with PMA was found to cause a considerable increase in the activation of p42/44 extracellular signal-regulated MAP kinases (ERK) and p38 MAP kinases, reaching a maximum at 30 min. In the presence of acLDL, the ERK inhibitor PD98059 decreased cholesterol esterification in HMDM by about 35%. In contrast, the p38 inhibitor SB203580 had no effect. However, when PMA was present in addition to SB203580, esterification was reduced to a level lower than that observed with PMA alone. These findings suggest that activation of ERK, but not p38, MAP kinases is involved in the induction of cholesterol esterification by acLDL in HMDM, while p38 MAP kinases may modulate the inhibitory effect of PKC, and thus provide evidence that MAP kinases play a role in the regulation of foam cell formation in human macrophages. |
| Cholesterol esterification in tissues and change in the apoprotein spectrum in rat blood under the effect of auto-oxidized cholesterol Dushkin, M. I., L. M. Poliakov, et al. (1991), Vopr Med Khim 37(5): 9-12. Abstract: Influence of autooxidized cholesterol (Ch) products on accumulation of cholesterol esters (ChE) in liver and aorta tissues as well as alteration of the apolipoprotein spectrum in low density and very low density (LDL and VLDL) lipoproteins in blood plasma was studied in rats treated with purified Ch (ChP-rats) and with oxidized Ch containing 5% 25-hydroxyCh and 3% 7-ketoCh (ChO-rats). Increase of ChE content in liver tissue of ChO-rats resulted in two-fold activation of acyl-CoA-cholesterol-O-acyltransferase (ACAT) in liver microsomes as compared with the enzymatic activity rate in ChP-rats. As shown by polyacrylamide gel electrophoresis content of apoE in VLDL and LDL of ChO-rats was 1,5-fold higher as compared with that of ChP-rats. Content of apoIV was increased in LDL and VLDL of ChP-rats as compared with controls; this effect was not observed in ChO-rats. LDL and VLDL from ChO-rats stimulated incorporation of 14C-oleate into ChE of cultivated macrophages. Increase in content of ChE found in aorta of ChO-rats appears to occur due to activation of Ch esterification. Intensification of ChE synthesis in tissues and alterations in the spectrum of LDL and VLDL apolipoproteins caused by oxidized products of cholesterol may be one of the mechanisms involved in atherogenesis. |
| Cholesterol esterification is not essential for secretion of lipoprotein components by HepG2 cells Graham, A., J. L. Wood, et al. (1996), Biochim Biophys Acta 1302(1): 46-54. Abstract: Hepatic acyl CoA:cholesterol acyltransferase (ACAT) activity may determine storage of cholesterol and supply of cholesteryl esters for the neutral lipid core of very low density lipoprotein. Inhibition of cholesterol esterification in HepG2 cells, by the ACAT inhibitor 447C88, partially reduced the secretion of labelled total cholesterol, but the secretion of apoprotein B mass, and of radiolabelled triacylglycerol and phosphatidylcholine were unaffected. Furthermore, this compound was shown to substantially deplete the intracellular cholesteryl ester mass without affecting secretion of lipoprotein components. In contrast, the less potent ACAT inhibitor, CL277,082, significantly decreased secretion of labelled triacylglycerol, phosphatidylcholine and total cholesterol, in a manner which mirrored the decreases in secretion of apoB. This study clearly illustrates that ACAT inhibitors can exert differential effects on secretion of apoB-containing lipoproteins, which do not correlate with their efficacy in inhibiting ACAT, arguing that cholesterol esterification is not essential for lipoprotein secretion from these cells. |
| Cholesterol esterification rate in plasma depleted of very low and low density lipoproteins is controlled by the proportion of HDL2 and HDL3 subclasses: study in hypertensive and normal middle-aged and septuagenarian men Dobiasova, M., J. Stribrna, et al. (1992), J Lipid Res 33(10): 1411-8. Abstract: The relationship between the fractional rate of cholesterol esterification (FERHDL) in very low density lipoprotein (VLDL)- and low density lipoprotein (LDL)-depleted plasma and the particle size distribution of high density lipoproteins (HDL) were studied in: a) a control group of 9 apparently healthy men (42 +/- 11 years); b) 15 septuagenarians (76 +/- 6 years) who had no clinical signs of coronary artery disease; and c) 32 outpatients with essential hypertension of different stages of severity (51 +/- 10 years). There were small differences between the groups with respect to their plasma total and HDL-cholesterol and plasma triglyceride levels. However, there was a highly significant increase in FERHDL in patients with hypertension compared to control and older men. The HDL of hypertensive patients had a markedly increased relative content of HDL3b, while their HDL2b fraction was reduced by over 50% compared to the other groups. Overall, there was a strong positive correlation between FERHDL and HDL3b (r = 0.89; P less than 0.001) and a negative correlation between FERHDL and HDL2b (r = -0.61; P less than 0.001) and HDL3a (r = -0.77; P less than 0.001). These findings confirm our previous conclusions that FERHDL reflects the relative HDL subclass distribution. In addition, we demonstrate that FERHDL is increased in hypertensive male subjects regardless of the stage of hypertension, i.e., whether or not organic lesions have already become manifest (stage III and stages I plus II, respectively). |
| Cholesterol esterification rates in very low density lipoprotein- and low density lipoprotein-depleted plasma. Relation to high density lipoprotein subspecies, sex, hyperlipidemia, and coronary artery disease Dobiasova, M., J. Stribrna, et al. (1991), Arterioscler Thromb 11(1): 64-70. Abstract: The fractional rate of cholesterol esterification in very low density lipoprotein- and low density lipoprotein-depleted plasma (FERHDL) was studied in normolipidemic subjects and in individuals with hyperlipidemia and proven coronary artery disease (CAD). The FERHDL was significantly higher than the FER in whole plasma and was significantly higher in normal men than in normal women. In addition, men and women with primary hyperlipidemia had significantly higher FERHDL values relative to their sex-matched controls. The most significant increases in FERHDL values, however, were observed in individuals with CAD. In all patient groups, FERHDL was positively correlated with plasma triglyceride concentration. In addition, FERHDL was negatively related to plasma high density lipoprotein (HDL) cholesterol concentration in all groups except in men with CAD and in normolipidemic women. The gradient gel electrophoretic pattern of HDL from individuals with either low or high FERHDL values indicated an inverse relation between this activity and the relative amount of HDL2b particles. FERHDL likely reflects the metabolic properties of the heterogeneous population of HDL particles in the plasma and may be a function of the relative content of larger and smaller HDL particles. It appears to be a sensitive and reliable functional measure of the particle size distribution in the HDL pool and one of potential clinical value in the assessment of risk for CAD. |