Cholesterol Journal Articles

Record 11021 to 11040

Reverse cholesterol transport in plasma of patients with different forms of familial HDL deficiency
von Eckardstein, A., Y. Huang, et al. (1995), Arterioscler Thromb Vasc Biol 15(5): 691-703.
Abstract: HDLs encompass structurally heterogenous lipoproteins that fulfill specific functions in reverse cholesterol transport. Two-dimensional nondenaturing gradient gel electrophoresis (2D-PAGGE) of normoalphalipoproteinemic plasma and subsequent immunoblotting with anti-apoA-I-antibodies differentiates pre-beta 1-LpA-I, pre-beta 2-LpA-I, pre-beta 3-LpA-I, alpha-LpA-I2, and alpha-LpA-I3. Immunodetection with anti-apoE antibodies differentiates gamma-LpE and alpha-LpE. Pulse-chase incubations of plasma with 3Hunesterified cholesterol (3HUC)-labeled fibroblasts and subsequent 2D-PAGGE revealed that cell-derived 3HUC is taken up by pre-beta 1-LpA-I and gamma-LpE. From these initial acceptors, 3HUC is transferred to LDL via pre-beta 2-LpA-I-->pre-beta 3-LpA-I-->alpha-LpA-I. Some UC is esterified in pre-beta 3-LpA-I, and some is esterified in alpha-LpA-I after its retransfer from LDL. In this study we investigated the effect of various forms of familial HDL deficiency on reverse cholesterol transport. Plasma samples of patients with various forms of HDL deficiency are characterized by the lack of specific HDL subclasses. ApoE-containing HDLs, including gamma-LpE, are present in all kinds of HDL deficiency. However, all forms of LpA-I are absent in apoA-I-deficient plasma, pre-beta 3-LpA-I and alpha-LpA-I from the plasma of patients with Tangier disease (TD), and pre-beta 3-LpA-I and large alpha-LpA-I from the plasma of patients with lecithin:cholesterol acyltransferase (LCAT) deficiency and fish-eye disease (FED). After a 1-minute pulse with labeled fibroblasts, efflux of 3HUC into HDL-deficient plasmas decreased, compared with normal plasma, by 49% (apoA-I deficiency), 36% (TD), 21% (LCAT deficiency), and 28% (FED). In apoA-I deficiency, only gamma-LpE takes up cell-derived 3HUC. In the three other HDL-deficiency states, cell-derived 3HUC is initially taken up by both pre-beta 1-LpA-I and gamma-LpE. The four HDL deficiencies are also characterized by differences in the esterification of cell-derived 3HUC. No esterification occurs in LCAT-deficient plasma. In FED plasma, 3HUC is esterified in LDL. In apoA-I deficiency and TD, however, 3HUC is esterified in lipoproteins free of apoA-I and apoB. In the two latter cases, the transfer of 3Hcholesteryl ester to LDL is enhanced compared with normal plasma. The lack of specific HDL subclasses and the consequent changes in reverse cholesterol transport pathways differently affect net mass efflux of cholesterol from fibroblasts into HDL-deficient plasma.(ABSTRACT TRUNCATED AT 400 WORDS)

Reverse cholesterol transport in the isolated perfused rat spleen
Mindham, M. A., P. A. Mayes, et al. (1990), Biochem J 268(2): 499-505.
Abstract: 1. A method has been developed which enables the rat spleen to be loaded in vivo with 3Hcholesterol to a high specific radioactivity using cholesterol-labelled erythrocytes. The erythrocytes were shown to be rapidly degraded by the spleen and not released intact during subsequent perfusion. 2. When labelled spleens were perfused with whole blood or serum, lipoproteins in the high-density lipoprotein (HDL) range were shown to be the principal lipoprotein vehicles for the removal of cholesterol, the specific radioactivity of cholesterol being much greater in the HDL fractions than in other lipoproteins, particularly in the d 1.175-1.210 fraction. 3. The formation of 3Hcholesteryl ester was restricted to the major HDL fractions. 4. Experiments utilizing individual HDL fractions added to a basal perfusate indicated that HDL1 (d 1.050-1.085) was of less importance in the removal of cholesterol from the spleen than HDL subfractions of higher density. Also, a decrease in density of the lipoproteins was observed during perfusion, concurrent with uptake of cholesterol, especially in the d 1.085-1.125 subfraction. 5. When 3Hcholesterol-labelled spleens were perfused with whole blood, about half of the radioactivity released was detected in erythrocytes, indicating a rapid exchange or transport of cholesterol. Thus erythrocytes could play an important role in the transfer of unesterified cholesterol when the chemical potential gradient is favourable.

Reverse cholesterol transport in the rat following a short-term intravenous infusion of fat emulsion
Wang, W. Q., X. D. Wang, et al. (1996), Pharmacol Toxicol 79(2): 49-54.
Abstract: The effect on cholesterol transport of an intravenous infusion of a fat emulsion (10%) Intralipid or 10% Lipovenos) in vivo was investigated in the rat. Intralipid (1.85 ml/hr/kg body weight in rts for 3 hr) caused a reduction (P < 0.05) in free cholesterol in the aorta (by 25%), in plasma high-density lipoproteins (64%) and in erythrocytes (11%) with a concomitant enrichment of liver free cholesterol (16%), suggesting an enhanced reverse cholesterol transport in this species. Lipovenos under the same conditions gave similar results. Our data support our previous in vivo study in man indicating that infusion of a fat emulsion is able even to remove cholesterol from the arterial wall and thereby possibly be considered as an antiatherosclerotic agent.

Reverse cholesterol transport in the rat. Studies using the isolated perfused spleen in conjunction with the perfused liver
Mindham, M. A. and P. A. Mayes (1991), Biochem J 279 (Pt 2): 503-8.
Abstract: 1. A new method combining the use of an isolated perfused extrahepatic tissue with a perfused liver was developed as a model system for the study of reverse cholesterol transport. Rat spleens, initially labelled in vivo with 3Hcholesterol, were perfused for 3 h with whole blood. The spleen was then replaced with an isolated rat liver, whose uptake of cholesterol from the spleen-derived blood and excretion of cholesterol into bile constituents were determined. 2. During spleen perfusion, a net release of cholesterol mass and radioactivity to lipoproteins was observed. 3. During liver perfusion, there was also a rapid exchange or transport of unesterified cholesterol between high-density lipoprotein (HDL) and the liver, in particular with HDL2 (d = 1.085-1.125). 4. The liver showed an increased uptake of cholesteryl ester from serum that had previously been used in spleen perfusion. 5. Approximately half of the 3Hcholesterol released by the spleen was recovered in erythrocytes. During subsequent liver perfusion there was a substantial uptake of radioactivity from the erythrocytes, although less than that recorded from serum lipoproteins. 6. In all experiments there was significant excretion of 3Hcholesterol into bile; most (85%) was in bile acids. Thus the complete process of reverse cholesterol transport is observed in this dual-perfusion system.

Reverse cholesterol transport in the rat: influence of short-term D-myo-inositol-1,2,6 trisphosphate (PP56) infusion
Wang, W. Q., X. D. Wang, et al. (1993), Pharmacol Toxicol 73(1): 49-51.
Abstract: D-myo-inositol-1,2,6 trisphosphate (PP56) was infused in rats for 3 hr at a rate of 30.28 microM/hr/kg body weight. The cholesterol content in plasma, erythrocytes, the aorta, and the liver was monitored before and at the end of the infusion and at 1 and 21 hr after the infusion. We found that the aortic total and free cholesterol content was reduced after the infusion and continuously until the end of the experiment (by 27% each after 21 hr P < 0.05, P < 0.01, respectively). Erythrocyte cholesterol was increased by 6.6% (P < 0.05) at the end of the infusion and 9.5% (P < 0.01) at the end of the experiment, while plasma and high-density lipoprotein cholesterol did not change significantly. Free cholesterol in the liver after infusion was decreased by 27% (P < 0.001) and cholesterol ester increased by 97% (P < 0.05) and did not return to the preinfusion level. Short-term PP56 infusion in the rat apparently influences cholesterol transport in a way which would suggest a promoted reverse cholesterol transport. Since the lipid values did not return to the preinfusion level, a long-term study is needed to elucidate in more detail the influence of PP56 on cholesterol metabolism in vivo.

Reverse cholesterol transport with acute exercise
Campaigne, B. N., R. N. Fontaine, et al. (1993), Med Sci Sports Exerc 25(12): 1346-51.
Abstract: Physical activity has been shown to be inversely related to coronary heart disease (CHD). The role of high density lipoprotein (HDL) particles in the process of reverse cholesterol transport may be a link between exercise and the prevention of CHD. The aim of the present study was to evaluate the effects of acute exercise on cholesterol efflux (C-EF) from human monocyte derived macrophages overloaded with cholesterol and subsequently incubated with HDL fractions isolated from plasma. Ten males; five sedentary (NR) and five runners (R) exercised 30 min on a cycle ergometer at 60% of maximum oxygen consumption. HDL-C was higher in R when compared with NR (49.2 +/- 2.6 vs 36.8 +/- 4.6 mg.dl-1; P < 0.05). Plasma lipid profiles did not differ between groups and were unchanged with exercise. C-EF was higher to HDL obtained from NR compared with R before exercise (1.05 +/- 0.17 vs 0.59 +/- 0.09 microgram/mg protein, P < 0.05). Acute exercise increased HDL's ability to act as an acceptor of cellular cholesterol in R, whereas it decreased in NR. These preliminary studies suggest that functional changes in HDL fractions may differ in NR and R, and appear to be influenced by acute exercise.

Reverse cholesterol transport, high density lipoproteins and HDL cholesterol: recent data
Fredenrich, A. and P. Bayer (2003), Diabetes Metab 29(3): 201-5.
Abstract: Unlike LDL cholesterol, which is a major cardiovascular risk factor, HDL cholesterol plays an important anti-atherogenic role through reverse cholesterol transport from peripheral cells to the liver. Some recent biochemical and epidemiological data shed light on this key function. In the hereditary Tangier disease with disseminated lipid storage, the main biochemical feature is a dramatically low level of HDL cholesterol. Different mutations in the ATP-binding cassette transporter A1 (ABCA1) gene have been recently described, which interfere with cellular cholesterol efflux. This results in low HDL plasma level, and defective reverse cholesterol transport to the liver. Moreover, selective hepatic uptake of HDL cholesteryl esters by SR-B1, a class B scavenger receptor, also plays a key role. In the follow-up of the PROCAM Study, the relative risk of coronary events is high in a cluster of patients with increased total cholesterol/HDL-cholesterol ratio. In the prospective secondary prevention VA-HIT study, the relative risk of coronary events in patients with low HDL cholesterol levels is decreased of 22% with a treatment by gemfibrozil. If the present available range of drugs targeted at increasing HDL cholesterol levels is rather narrow, future therapies will be encouraging, especially with agonists of PPARs.

Reverse cholesterol transport: high-density lipoprotein's magnificent mile
Toth, P. P. (2003), Curr Atheroscler Rep 5(5): 386-93.

Reverse cholesterol transport: its contribution to cholesterol catabolism in normal and disease states
Loh, K. C. and M. H. Tan (1996), Can J Cardiol 12(10): 944-50.
Abstract: OBJECTIVES: To review the reverse cholesterol transport (RCT) model and its contribution to cholesterol catabolism in normal and disease states. DATA SOURCES: Pertinent articles were identified through a MEDLINE search of the English language literature from 1983 to 1995, followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Review articles, laboratory and clinical studies and case reports. DATA EXTRACTION: The physiology of the RCT pathway as well as alterations observed in individuals with diseases or lifestyle changes were reviewed. DATA SYNTHESIS: Data were derived mainly from laboratory studies and clinical observations. The RCT model is proposed to explain the removal of excess cholesterol from extrahepatic tissues and its delivery to liver for catabolism. This involves several regulated steps mediated by the plasma apolipoproteins and two key enzymes, lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). In essence free cholesterol in peripheral tissues is taken up by nascent high density lipoprotein (HDL) particles, converted to cholesteryl esters (by LCAT), and then transferred to apo B-containing lipoproteins (by CETP) for hepatic removal. Altered cholesterol catabolism may occur in individuals with disorders of a genetic or acquired nature as well as lifestyle changes, as a result of alterations in one of several of the putative steps or enzymes involved in RCT. CONCLUSIONS: The proposed antiatherogenic role of RCT remains to be validated as a review of the possible alterations noted in various disorders showed conflicting results in atherogenic propensity.

Reverse cholesterol transport: physiology and pharmacology
Franceschini, G., P. Maderna, et al. (1991), Atherosclerosis 88(2-3): 99-107.
Abstract: Reverse cholesterol transport identifies a series of metabolic events resulting in the transport of cholesterol from peripheral tissues to the liver and plays a major role in maintaining cholesterol homeostasis in the body. High density lipoproteins (HDL) are the vehicle of cholesterol in this reverse transport, a function believed to explain the inverse correlation between plasma HDL levels and atherosclerosis. An attempt to stimulate, by the use of drugs, this transport process seems to be of great promise in the prevention and treatment of arterial disease. Only few drugs are now known that can modify the activity of the various factors involved in the process. Clofibrate reduces cholesterol esterification, but the newer fibric acids are generally ineffective as anion-exchange resins. Probucol directly increases the activity and mass of cholesteryl ester transfer protein, thus possibly improving the physiological process of cholesterol removal from tissues. The few available data on the effects of drugs on reverse cholesterol transport should stimulate the search for new agents specifically stimulating this antiatherogenic process.

Reverse cholesterol transport: relationship between free cholesterol uptake and HDL3 in normolipidaemic and hyperlipidaemic subjects
Cabezas, M. C., G. P. Van Heusden, et al. (1993), Eur J Clin Invest 23(2): 122-9.
Abstract: High density lipoproteins (HDL) are responsible for the Reverse Cholesterol Transport (RCT). The role of the composition of the HDL particle in RCT, involving free cholesterol (chol) uptake from cell membranes, is not completely understood. We have therefore studied the uptake capacity from subjects with a wide variety of plasma HDL cholesterol concentrations in an HDL-receptor free model consisting of bovine heart mitochondrial membranes labeled with 14Ccholesterol. HDL were isolated by molecular sieve chromatography from fresh plasma samples of eight subjects with low plasma HDL chol concentrations (< or equal to 1.0 mmol L-1) and 15 subjects with normal HDL chol concentrations. The latter were subdivided into an intermediate (HDL chol: 1.0-1.4 mmol L-1; n =9) and a high HDL chol group (> or equal to 1.4 mmol L-1; n = 6). In the HDL fractions isolated by chromatography (cHDL), total chol and apolipoprotein (apo) AI were measured. Free chol uptake was significantly decreased by 32% in the tertile with the lowest plasma HDL chol (49.1 +/- 15.8 arbitrary units; mean +/- SD), compared to the tertile with high HDL chol (72.1 +/- 16.6 au). Linear regression analysis showed a positive correlation between the free chol uptake and plasma HDL3 concentrations (r = 0.61; P < 0.01), HDL chol (r = 0.56; P < 0.01), HDL associated apo AI (R = 0.46; P < 0.05), cHDL apo AI (r = 0.56; P < 0.05) and cHDL chol (r = 0.46; P < 0.05) in all subjects combined. Stepwise multiple-regression analysis confirmed the association of 14C cholesterol uptake with plasma HDL3 concentrations (beta, 0.61; P = 0.004). No correlations were found between free chol uptake and total plasma apo AI (r = 0.26. ns) or HDL2 (r = 0.27; ns). After an oral fat load in four FCH patients, free chol uptake paralleled the changes in plasma HDL 3 chol concentrations. We conclude that HDL3 is involved in the early steps of RCT and low HDL 3 levels may result in less efficient RCT in hypertriglyceridemia.

Reverse cholesterol transport--a review of the process and its clinical implications
Hill, S. A. and M. J. McQueen (1997), Clin Biochem 30(7): 517-25.
Abstract: OBJECTIVES: This review article will summarize the current knowledge surrounding the reverse cholesterol transport system; the process, the effect of mutations in genes coding for proteins which function in the system, and the possible clinical implications of these alterations. RESULTS: High-density lipoprotein-cholesterol (HDL-C) concentration is a marker for the reverse cholesterol transport (RCT) system, whereby cholesterol is returned from peripheral cells to the liver for reuse or excretion in the bile. Increased HDL-C concentrations are generally accepted to be protective against the future development of atherosclerosis and coronary artery disease (CAD), but recent evidence has indicated that the underlying cause of the increased HDL-C may affect whether it is protective or detrimental. The major steps in the RCT pathway are the efflux of free cholesterol from cells and binding by pre-beta HDL, esterification of HDL-bound cholesterol by lecithin cholesterol acyl transferase (LCAT), cholesteryl ester transfer protein (CETP) mediated exchange of cholesteryl ester and triglycerides between HDL and apo B-containing particles, and hepatic lipase (HL) mediated uptake of cholesterol and triglycerides by the liver. Mutations in proteins active in the RCT pathway can shed light on the functions and control of the various steps in the system. LCAT deficiency, leading to greatly reduced HDL and fish eye disease, is not usually associated with increased risk of CAD. Several new mutations in LCAT have recently been reported, however, which do result in CAD. Mutations leading to reduced CETP activity result in less CE being directed into apo-B containing particles and more remaining in the HDL. This has been associated with increased HDL-C concentrations. The generally accepted hypothesis that reduced CETP activity leads to reduced CAD risk has been challenged by a number of recent publications, and has become an area of active investigation. Mutations leading to reduced HL activity are rare occurrences. To date, all have been associated with increased HDL-C concentrations and CAD. CONCLUSION: The development of techniques to identify and characterize the functional significance of mutations in proteins involved in RCT will aid in the understanding of the mechanisms and control of this pathway.

Reverse micelle formation for acceleration of the supercritical fluid extraction of cholesterol from food samples
Jimenez-Carmona, M. M. and M. D. Luque de Castro (1998), Anal Chem 70(10): 2100-3.
Abstract: Reverse micelle formation is presented as a new strategy for improving the extraction of polar species with supercritical (SC) CO2. The addition of a reverse-micelleforming reagent prior to SFE accelerates the quantitative extraction of the analyte. The effect was used to develop a method for the determination of cholesterol in solid foods. The proposed method involves the addition of a microemulsion of a nonionic surfactant (Triton X-100) to the sample and dynamic extraction with SC-CO2 at 383 bar and 40 degrees C for 20-40 min. The method was validated using a certified reference material (NIST-SRM 1845) and was subsequently used to analyze low-cholesterol (whole bread, oat biscuits, orange biscuits) and high-cholesterol foods (semiskimmed and whole milk) with excellent results (RSD < 11% in all instances).

Reversibility of atherosclerosis--evolving perspectives from two arterial imaging clinical trials: the cholesterol lowering atherosclerosis regression study and the monitored atherosclerosis regression study
Hodis, H. N. (1995), J Cardiovasc Pharmacol 25 Suppl 4: S25-31.
Abstract: The Cholesterol Lowering Atherosclerosis Study (CLAS) and the Monitored Atherosclerosis Regression Study (MARS) are serial arterial imaging clinical trials that have explored the reversibility of atherosclerosis with lipid-lowering therapy in native coronary, carotid, and femoral arterial beds, as well as in coronary artery bypass grafts. Results demonstrate that progression of atherosclerosis can be reduced in all these vascular beds. Evolving data indicate that coronary lesions > or = 50% diameter stenosis (%S) at baseline respond more readily to lipid-lowering therapy than lesions <50%S. In addition, lipoproteins may have a differential effect on coronary lesion progression according to lesion size, with triglyceride-rich lipoproteins playing an important role in the progression of lesions <50%S. Limited data indicate that progression of atherosclerosis in women may be more responsive to lipid-lowering therapy than in men, and that estrogen replacement may enhance the anti-atherosclerosis effects of lipid lowering. Longitudinal measurements of carotid artery far wall intima-media thickness (IMT) with B-mode ultrasonography in CLAS and MARS indicate that carotid atherosclerosis at a stage before lesions intrude into the vessel lumen can be reduced by lipid-lowering therapy. Together, CLAS and MARS data indicate that the spectrum from very early lesions confined to the arterial wall to established lesions late in the atherosclerotic process can be reversed with lipid-lowering therapy.

Reversible covalent attachment of cholesterol to oligodeoxyribonucleotides for studies of the mechanisms of their penetration into eucaryotic cells
Boutorine, A. S. and E. V. Kostina (1993), Biochimie 75(1-2): 35-41.
Abstract: A method in which a cholesterol moiety was covalently attached to oligonucleotides via a disulfide bond has been proposed as a means for studying the penetration of oligonucleotides into living cells. This bond may be cleaved by a mild treatment with thiol-containing reagents during some stages of the uptake process. Attachment of the cholesterol moiety resulted in a 30-50-fold increase in uptake of the oligonucleotide derivative by T24 human carcinoma cells. However, more than 80% of the oligonucleotide derivative remained on the external surface of the cellular membrane. Within the cytoplasm, the oligonucleotide derivatives were found in endosome-like vesicles which were observed during the first 6 h following treatment. Oligonucleotide moieties never cross the membrane, and endocytosis, with or without receptors, is the principal mechanisms for cellular uptake. Only about 15% of the oligonucleotides that penetrated the cells were found in the nuclear fraction. Treatment of the cells with dithiothreitol resulted in a release of most of the cell-associated oligonucleotide derivatives from the external surface of the membrane, but did not change the chemical state or intracellular distribution of the penetrated oligonucleotide derivatives. Mechanisms of the binding of cholesterol-modified oligonucleotides to cellular membranes, non-receptor mediated endocytosis and the role oligonucleotide transportation mechanisms play in determining the fate of penetrated oligonucleotides within the cell are discussed.

Reversible effects of sphingomyelin degradation on cholesterol distribution and metabolism in fibroblasts and transformed neuroblastoma cells
Porn, M. I. and J. P. Slotte (1990), Biochem J 271(1): 121-6.
Abstract: Plasma-membrane sphingomyelin appears to be one of the major determinants of the preferential allocation of cell cholesterol into the plasma-membrane compartment, since removal of sphingomyelin leads to a dramatic redistribution of cholesterol within the cell Slotte & Bierman (1988) Biochem. J. 250, 653-658. In the present study we examined the long-term effects of sphingomyelin degradation on cholesterol redistribution in cells and determined the reversibility of the process. In a human lung fibroblast-cell line, removal of 80% of the sphingomyelin led to a rapid and transient up-regulation (3-fold) of acyl-CoA:cholesterol acyltransferase (ACAT) activity, and also, within 30 h, to the translocation of about 50% of the cell non-esterified cholesterol from a cholesterol oxidase-susceptible compartment (i.e. the cell surface) to oxidase-resistant compartments. At 49 h after the initial sphingomyelin degradation, the cell sphingomyelin level was back to 45% of the control level, and the direction of cell cholesterol flow was toward the cell surface, although the original distribution was not achieved. In a transformed neuroblastoma cell line (SH-SY5Y), the depletion of sphingomyelin led to a similarly rapid and transient up-regulation of ACAT activity, and to the translocation of about 25% of cell-surface cholesterol into internal membranes (within 3 h). The flow of cholesterol back to the cholesterol oxidase-susceptible pool was rapid, and a pretreatment cholesterol distribution was reached within 20-49 h. Also, the resynthesis of sphingomyelin was faster in SH-SY5Y neuroblastoma cells and reached control levels within 24 h. The findings of the present study show that the cellular redistribution of cholesterol, as induced by sphingomyelin degradation, is reversible and suggest that the normalization of cellular cholesterol distribution is linked to the re-synthesis of sphingomyelin.

Review article: in vitro studies of gall-bladder smooth muscle function. Relevance in cholesterol gallstone disease
Portincasa, P., F. Minerva, et al. (2000), Aliment Pharmacol Ther 14 Suppl 2: 19-26.
Abstract: The interplay between contraction and relaxation in the gall-bladder muscularis leads to appropriate gall-bladder emptying and refilling during fasting and in the postprandial state in vivo. Several studies in both human and animal models have focused on cellular and molecular events in the gall-bladder wall in health and disease in vitro. Principal methods to study gall-bladder smooth muscle function include receptor binding studies (at the level of plasmamembranes or histological sections), phase contrast microscopy (at the level of isolated smooth muscle cells), and tensiometry (at the level of smooth muscle strips or the whole gall-bladder). At a very early stage, cholesterol gallstone disease is characterized by exposure of the gall-bladder wall to excess of biliary cholesterol and the cytotoxic effect of the bile salt deoxycholate. On a long-term basis, a form of gall-bladder leiomyopathy develops with defects involving the mechanisms of signal transduction at the level of plasmamembranes. The end-stage result is pathological contraction and/or relaxation of smooth musculature, impaired gall-bladder motility and gall-bladder stasis, all key factors in the pathogenesis of biliary cholesterol crystallization and gallstones.

Review of 5 years of a combined dietary and physical fitness intervention for control of serum cholesterol
Angotti, C. M. and M. S. Levine (1994), J Am Diet Assoc 94(6): 634-8; quiz 639-40.
Abstract: A chart review covering the first 5 years of clinical experience with a combined dietary and exercise intervention program for the reduction of hypercholesterolemia at the National Aeronautics and Space Administration headquarters demonstrated the program's success in maintaining high-density lipoprotein cholesterol (HDL-C) levels while significantly lowering total serum cholesterol levels. This combined program also resulted in improved ratios of total serum cholesterol to HDL-C and lowered levels of low-density lipoprotein cholesterol, thus further reducing the risk for cardiovascular disease. The National Aeronautics and Space Administration Cardiovascular Risk Reduction Program was developed after it was determined that although dietary intervention alone improved total cholesterol levels, it often resulted in a more than proportionate decrease in HDL-C and a worsening of the ratio of cholesterol to HDL-C. An approach was needed that would positively affect all factors of the lipid profile. The findings from the program indicate that reduction of cardiovascular risk can be accomplished easily and effectively at the worksite through dietary intervention, personal monitoring, and a reasonable exercise program.

Review of cholesterol absorption with emphasis on dietary and biliary cholesterol
Wilson, M. D. and L. L. Rudel (1994), J Lipid Res 35(6): 943-55.

Review of cholesterol-lowering therapy: coronary angiographic and events trials
Waters, D. and T. R. Pedersen (1996), Am J Med 101(4A): 4A34S-38S; discussion 39S.
Abstract: Coronary angiographic trials have demonstrated that the lowering of cholesterol slows the progression of atherosclerosis, enhances atherosclerotic regression, limits the formation of new lesions, and reduces the incidence of coronary events. Atherosclerotic progression has been shown to be associated with an increased risk of cardiac death, cardiac death plus nonfatal myocardial infarction (MI), and all coronary events. Most of the atherosclerotic regression trials were too small and of too short duration to demonstrate a significant difference in hard coronary events between patients receiving cholesterol-lowering intervention and controls. However, when data from these studies were pooled, total mortality was found to be reduced by 26% and the rate of nonfatal MI by 39% in actively treated patients. The first events trial to demonstrate clearly a reduction in overall mortality was the Scandinavian Simvastatin Survival Study (4S), in which lowering of serum cholesterol in patients with coronary artery disease (CAD) and hypercholesterolemia also reduced coronary mortality, fatal and nonfatal MI, sudden cardiac death, and the need for revascularization. Reductions in major coronary events were seen consistently in all subgroups of patients studied and regardless of concomitant therapy with aspirin, beta blockers, or calcium antagonists. Further evidence of the benefit of cholesterol-lowering therapy was provided by the West of Scotland Coronary Prevention Study (WOSCOPS), which evaluated men with hypercholesterolemia but no history of CAD. Those receiving active treatment had less overall mortality, lower risk of definite nonfatal MI or death from definite or suspected CAD, and less need for revascularization. The Cholesterol and Recurrent Events (CARE) Study recently showed that lipid-lowering therapy is also beneficial in CAD patients with less severe dyslipidemia.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles