Cholesterol Journal Articles

Record 4581 to 4600

Dose-dependent suppression of transplant arteriosclerosis in aorta-allografted, cholesterol-clamped rabbits. Suppression not eliminated by the cholesterol-raising effect of cyclosporine
Andersen, H. O., P. Holm, et al. (1997), Arterioscler Thromb Vasc Biol 17(11): 2515-23.
Abstract: Cyclosporine may suppress transplant arteriosclerosis; however, it also raises plasma cholesterol, which could promote the disease. Our aim was to test these hypotheses experimentally. In experiment 1 (n = 34), cholesterol was clamped at a human level of 5 to 7 mmol/L, and rabbits were given either saline or cyclosporine in a low, medium or high dose. In experiment 2 (n = 15), in which dietary cholesterol was fixed at 0.05 g.kg-1.d-1, and experiment 3 (n = 16), in which no dietary cholesterol was added to the chow, rabbits were given either medium-dose cyclosporine, saline, or vehicle. The duration of each experiment was 5 weeks. In experiment 1, cyclosporine attenuated the development of transplant arteriosclerosis dose dependently (trend test: P <.0001). Cyclosporine also suppressed, in a dose-dependent manner, the activation of the immune system (trend test: P <.05) and the presence of T lymphocytes (trend test: P <.0001) and macrophages in the intima (trend test: P <.01). Despite a higher plasma cholesterol level in cyclosporine-treated rabbits compared with saline-treated rabbits in both experiment 2 (4.9 versus 2.9 mmol/L) and experiment 3 (1.6 versus 0.8 mmol/L), transplant arteriosclerosis was significantly reduced by cyclosporine (Mann-Whitney U test; P <.05 and P <.05). These results suggest that cyclosporine suppresses experimental transplant arteriosclerosis dose dependently. Accordingly, in the assessment of the optimal cyclosporine dose to heart-transplanted patients, it should be taken into account that a dose reduction may promote transplant arteriosclerosis.

Dose-related increase of HDL-cholesterol levels after N-acetylcysteine in man
Franceschini, G., J. P. Werba, et al. (1993), Pharmacol Res 28(3): 213-8.
Abstract: Changes in plasma lipid-lipoprotein levels were evaluated in 10 hyperlipidemic patients during treatment with progressive doses (from 1200 mg day-1 to 3600 mg day-1) of N-acetylcysteine (NAC). Plasma total cholesterol and triglyceride levels, as well as those of lipoprotein (a) did not change to an appreciable extent, even with the highest dosage. However, the HDL-cholesterol levels showed a significant, dose-related rise, the mean absolute increase, with the highest NAC dose, being of approximately 10 mg dl-1 (16.2%). The rise of HDL-cholesterol was independent of changes in other lipid-lipoprotein parameters, suggesting a possible direct effect of NAC on the HDL system.

Dose-response effects of atorvastatin and simvastatin on high-density lipoprotein cholesterol in hypercholesterolaemic patients: a review of five comparative studies
Wierzbicki, A. S. and D. P. Mikhailidis (2002), Int J Cardiol 84(1): 53-7.
Abstract: Epidemiological evidence and clinical trials with fibrate therapy show a clear relationship between low levels of high-density lipoprotein cholesterol (HDL-C) and cardiovascular risk. In addition to lowering plasma levels of low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG), the hydroxy-methylglutaryl-coenzyme A reductase inhibitors (statins), also raise the levels of HDL-C. This review summarizes the results of five randomized, multicenter studies in hypercholesterolaemic patients in which multiple doses of atorvastatin and simvastatin were compared for their effects on lipids and lipoproteins including HDL-C. Both statins reduced LDL cholesterol and achieved parallel decreases in TG, with atorvastatin showing a slight overall superiority in these studies. Both HDL-C and apolipoprotein (Apo) A-I, its associated apoprotein, were significantly and consistently increased by all doses of simvastatin. However, atorvastatin had a different dose-response effect from simvastatin on both lipid parameters. Whereas HDL-C and Apo A-I were elevated by low doses of atorvastatin, the effect diminished markedly with increasing dose suggesting a possible negative dose-response effect. At higher doses, simvastatin increased HDL-C and Apo A-I significantly more than atorvastatin. These data indicate that statins may not be identical in all their clinical properties relevant to reducing the risks of atherosclerosis.

Double-blind, randomized feedback control fails to improve the hypocholesterolemic effect of a plant-based low-fat diet in patients with moderately elevated total cholesterol levels
Koebnick, C., S. Plank-Habibi, et al. (2004), Eur J Clin Nutr 58(10): 1402-9.
Abstract: OBJECTIVE: To determine whether the cholesterol-lowering effect of a plant-based low-fat diet can be improved by a flexible control design that controls the extent of fat reduction based on the individual response of blood cholesterol. DESIGN: Randomized, double-blind intervention study. SETTING: A hotel in Prerow, Germany. SUBJECTS: A total of 32 participants (21 female and 11 male participants) with total cholesterol level > 5.7 mmol/l. INTERVENTION: The control group consumed a plant-based low-fat diet with constantly 20% of energy as fat; the intervention group received a diet with either 20 or 15% of energy as fat, depending on the serum cholesterol response of the preceding week. A flexible control design based on the individual cholesterol response during a run-in period of 1 week was used within a low-fat intervention. RESULTS: During the run-in period, the consumption of a plant-based low-fat diet led to a reduction in total cholesterol by 18+/-6 mmol/l (P < 0.001), in LDL cholesterol by 19+/-9 mmol/l (P < 0.001) and triglycerides by 13+/-3 mmol/l (P < 0.001). During the feedback control period, an additional reduction in total cholesterol by 13+/-8 (P < 0.001) and in LDL cholesterol by 17+/-11 (P < 0.001) was observed compared to 15+/-15 and 7+/-18 in the control group. The effect of an additional feedback control was only marginal and not statistically significant compared to the effect of the low-fat diet alone. CONCLUSIONS: On a level of fat intake already reduced to 20% of energy, the use of a feedback control to adapt the fat content of the diet depending on the individual serum cholesterol response was not more effective in reducing blood cholesterol levels than a plant-based low-fat diet alone.

Doubtful advices on cholesterol screening in children
Ravnskov, U. (1993), Ugeskr Laeger 155(24): 1886-7.

Down with the bad, up with the good. A biotech firm develops a vaccine to raise good cholesterol levels
Maeder, T. (2002), Sci Am 286(2): 32-3.

Down-regulation of cholesterol biosynthesis in sitosterolemia: diminished activities of acetoacetyl-CoA thiolase, 3-hydroxy-3-methylglutaryl-CoA synthase, reductase, squalene synthase, and 7-dehydrocholesterol delta7-reductase in liver and mononuclear leukocytes
Honda, A., G. Salen, et al. (1998), J Lipid Res 39(1): 44-50.
Abstract: Sitosterolemia is a recessively inherited disorder characterized by abnormally increased plasma and tissue plant sterol concentrations. Patients have markedly reduced whole body cholesterol biosynthesis associated with suppressed hepatic, ileal, and mononuclear leukocyte 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-controlling enzyme in cholesterol biosynthetic pathway, coupled with significantly increased low density lipoprotein (LDL) receptor expression. To investigate the mechanism of down-regulated cholesterol biosynthesis, we assayed several other key enzymes in the cholesterol biosynthetic pathway including acetoacetyl-CoA thiolase, HMG-CoA synthase, squalene synthase, and 7-dehydrocholesterol delta7-reductase activities in liver and freshly isolated mononuclear leukocytes from four sitosterolemic patients and 19 controls. Hepatic acetoacetyl-CoA thiolase, HMG-CoA synthase, reductase, and squalene synthase activities were significantly decreased (P < 0.05) -39%, -54%, -76%, and -57%, respectively, and 7-dehydrocholesterol delta7-reductase activity tended to be lower (-35%) in the sitosterolemic compared with control subjects. The reduced HMG-CoA synthase, reductase, and squalene synthase activities were also found in mononuclear leukocytes from a sitosterolemic patient. Thus, reduced cholesterol synthesis is caused not only by decreased HMG-CoA reductase but also by the coordinate down-regulation of entire pathway of cholesterol biosynthesis. These results suggest that inadequate cholesterol production in sitosterolemia is due to abnormal down-regulation of early, intermediate, and late enzymes in the cholesterol biosynthetic pathway rather than a single inherited defect in the HMG-CoA reductase gene.

Down-regulation of hepatic HMG-CoA reductase in mice by dietary cholesterol: importance of the delta 5 double bond and evidence that oxidation at C-3, C-5, C-6, or C-7 is not involved
Lund, E. and I. Bjorkhem (1994), Biochemistry 33(1): 291-7.
Abstract: It has been suggested that the down-regulation of hepatic HMG-CoA reductase by dietary cholesterol requires modification of the cholesterol molecule before it can exert its suppressive action. In a recent study Lund, E., Breuer, O., & Bjorkhem, I. (1992) J. Biol. Chem. 267, 25092-25097, we showed that side-chain hydroxylation is not likely to be of importance for this down-regulation in male C57BL/6J mice. In this study, we studied the possibility that modification of cholesterol in the region around the delta 5 double bond is required for the suppression. It was shown that cholestanol, which does not have a delta 5 double bond but is otherwise identical to cholesterol, is a poor suppressor of HMG-CoA reductase activity. Groups of mice were fed with diets containing cholestanol, epicholesterol, 6-methylcholesterol, 6-fluorocholesterol, 3 alpha-2Hcholesterol, and 7,7-2H2cholesterol with control groups fed cholesterol or a cholesterol-free diet. These cholesterol analogues were selected to interfere with potential in vivo modifications and to clarify structural requirements for the down-regulation. After sacrifice, the hepatic HMG-CoA reductase activity was assayed. Cholesterol, 6-methylcholesterol, and 6-fluorocholesterol were efficient suppressors whereas cholestanol and epicholesterol only had a low suppressive capacity. Differences in the degree of absorption from the intestine or degree of esterification were too small to explain the differences in HMG-CoA reductase suppressing capacity. The two deuterated cholesterol species had a suppressive capacity similar to that of unsubstituted cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Down-regulation of hepatic lecithin:cholesterol acyltransferase gene expression in chronic renal failure
Vaziri, N. D., K. Liang, et al. (2001), Kidney Int 59(6): 2192-6.
Abstract: BACKGROUND: Chronic renal failure (CRF) is associated with premature arteriosclerosis, impaired high-density lipoprotein (HDL) maturation, increased pre-beta HDL (a lipid-poor HDL species), reduced HDL/total cholesterol ratio, hypertriglyceridemia, and depressed lipolytic activity. The latter has been, in part, attributed to elevated pre-beta HDL, which is a potent inhibitor of lipoprotein lipase (LPL). Accumulation of cholesterol in the arterial wall is a critical step in atherogenesis, and HDL-mediated cholesterol removal from peripheral tissues mitigates atherosclerosis. Lecithin:cholesterol acyltransferase (LCAT) is essential for maturation of HDL and cholesterol removal by HDL from peripheral tissues. Earlier studies have revealed depressed plasma LCAT enzymatic activity in patients with CRF. This study was conducted to determine whether impaired LCAT activity can be confirmed in CRF animals and if so whether it is due to down-regulation of hepatic LCAT expression. METHODS: Hepatic tissue LCAT mRNA and plasma LCAT enzymatic activity were measured in male Sprague-Dawley rats six weeks after excisional 5/6 nephrectomy or sham operation. RESULTS: Compared with the controls, the CRF group exhibited a significant reduction of hepatic tissue LCAT mRNA abundance. The reduction in hepatic LCAT mRNA was accompanied by a marked reduction of plasma LCAT activity and elevation of serum-free cholesterol in the CRF animals. LCAT activity correlated positively with the HDL/total cholesterol ratio and inversely with free cholesterol and triglyceride concentrations. CONCLUSIONS: CRF leads to a marked down-regulation of hepatic LCAT mRNA expression and plasma LCAT activity. This abnormality can impair HDL-mediated cholesterol uptake from the vascular tissue and contribute to cardiovascular disease. In addition, LCAT deficiency can, in part, account for elevated serum-free cholesterol, reduced HDL/total cholesterol, and elevated pre-beta HDL in CRF. The latter can, in turn, depress lipolytic activity and hinder triglyceride-rich lipoprotein clearance in CRF.

Down-regulation of mammalian 3-hydroxy-3-methylglutaryl coenzyme A reductase activity with highly purified liposomal cholesterol
Plemenitas, A. and J. A. Watson (1999), Eur J Biochem 266(2): 317-26.
Abstract: Chinese hamster ovary-215 cells (CHO-215) cannot synthesize C27 and C28 sterols because of a defect in the reaction that decarboxylates 4-carboxysterols Plemenitas, A., Havel, C.M. & Watson, J.A. (1990) J. Biol. Chem. 265, 17012-17017. Thus, CHO-215 cell growth is dependent on an exogenous metabolically functional source of cholesterol. We used CHO-215 cells to (a) determine whether highly purified (> 99.5%) cholesterol, in egg lecithin liposomes, could down-regulate derepressed 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and if so (b) determine whether the loss in reductase catalytic activity correlated kinetically with the synthesis and accumulation of detectable oxycholesterol derivatives. Liposomal cholesterol (26-39 microM) supported maximum CHO-215 growth and initiated suppression of HMG-CoA reductase activity at concentrations greater than 50 microM. Maximum suppression (50-60%) of reductase activity was achieved with 181.3 microM liposomal cholesterol in 6 h. Also, regulatory concentrations of highly purified liposomal 3Hcholesterol were not converted (biologically or chemically) to detectable levels of oxy3Hcholesterol derivatives during 3-6 h incubations. Lastly, a broad-spectrum cytochrome P450 inhibitor (miconazole) had no effect on liposomal cholesterol-mediated suppression of HMG-CoA reductase activity. These observations established that (a) highly purified cholesterol, incorporated into egg lecithin liposomes, can signal the down-regulation of derepressed mammalian cell HMG-CoA reductase activity and (b) if oxycholesterol synthesis was required for liposomal cholesterol-mediated down-regulation, the products had to be more potent than 24-, 25-, or 26-/27-hydroxycholesterol.

Doxazosin reduces prevalence of small dense low density lipoprotein and remnant-like particle cholesterol levels in nondiabetic and diabetic hypertensive patients
Hirano, T., G. Yoshino, et al. (2001), Am J Hypertens 14(9 Pt 1): 908-13.
Abstract: Small dense low density lipoprotein (LDL) and remnant lipoproteins are potent atherogenic lipoproteins, often elevated in the plasma of patients with type 2 diabetes. The alpha1-blocker doxazosin has been reported to favorably affect the plasma lipid profile. We examined whether doxazosin could reduce these atherogenic lipoproteins in hypertensive subjects with and those without type 2 diabetes. Seventeen nondiabetic hypertensive patients and 33 hypertensive patients with type 2 diabetes were studied. Doxazosin (2 to 4 mg) was administered alone or with other previously received antihypertensive drugs for 6 months. Mean LDL size was measured by 2% approximately 16% gradient gel electrophoresis. Remnant-like particle (RLP)-cholesterol was measured with the use of an affinity column containing anti-apoA1 and B100 monoclonal antibodies. Doxazosin effectively decreased blood pressure (BP) without significantly affecting glucose, glycosylated hemoglobin (HbA1c), or C-peptide levels in both nondiabetic and diabetic patients. Doxazosin significantly reduced triglyceride, apo CIII, and apo B, but did not alter total-, LDL- or HDL-cholesterol. Mean LDL particle diameter was significantly increased from 25.6+/-0.6 nm to 25.9+/-0.4 nm (P <.001) by doxazosin treatment, regardless of the presence of diabetes. Consequently, the prevalence of small dense LDL (<25.5 nm) was halved in both groups. The increase in LDL size significantly correlated with decrease in triglyceride level (r=-0.798, P <.0001). Doxazosin significantly reduced RLP-cholesterol in both groups. These results suggest that doxazosin may help to prevent coronary artery disease by reducing atherogenic lipoproteins, including small dense LDL and remnant lipoproteins, in hypertensive patients, regardless of the presence of diabetes.

Dramatic changes in the serum levels of anti-cholesterol antibodies after eversion endarterectomy in patients with severe carotid atherosclerosis
Biro, A., E. Dosa, et al. (2005), Immunol Lett 99(1): 51-6.
Abstract: Our goal was to study changes in anti-cholesterol antibodies (ACHA) levels in patients with severe carotid stenosis after eversion endarterectomy. Seventy consecutive patients who underwent eversion endarterectomy at the Department of Cardiovascular Surgery, Semmelweis University, Budapest, were included in the study. Serum samples from 66 healthy volunteers served as controls. Patients had medical check up at 5.7 (4.6-8.0) weeks (median (interquartile range)), 6.8 (6.2-7.9) months as well as 13.8 (12.3-19.0) months after endarterectomy. In all patients the carotid arteries were investigated by color duplex ultrasound. ACHA concentrations were determined in the serum samples taken before operation as well as at the first and last follow-up visits by using an ELISA method. ACHA concentrations (median (interquartile range) were found to be significantly (p<0.0001) lower in the sera of the patients with carotid atherosclerosis (13.5 (8.4-21.3)AU/ml) than in the healthy subjects (26.1 (20.9-33.2)AU/ml) (Mann-Whitney test). Strong negative correlation was found between the preoperative ACHA and LDL-cholesterol levels (r=-0.413, p=0.0004). Serum ACHA concentrations significantly (p<0.0001) increased from the values measured before operation (13.5 (8.4-21.3)AU/ml) to 27.1 (19.9-34.7)AU/ml measured at the end of the 14 months long follow-up. Increase occurred only in patients with low or medium baseline ACHA concentration. Our present findings indicate that after surgical removal of atherosclerotic plaques from the carotid arteries the reduced baseline levels of ACHA reach normal values in 1 year. Different not mutually exclusive mechanisms (binding of ACHA to lipid/lipoproteins particles, to advanced plaques or reversibly injured endothelial cells in CNS) can be responsible for this novel finding.

Dramatic differences in lipoprotein composition among gray short-tailed opossums (Monodelphis domestica) fed a high cholesterol/saturated fat diet
Rainwater, D. L. and J. L. VandeBerg (1992), Biochim Biophys Acta 1126(2): 159-66.
Abstract: Lipoproteins of gray short-tailed opossums (Monodelphis domestica) were characterized to determine the basis of differences among individuals in response to a challenge diet enriched in saturated fat and cholesterol. Animals were selected from two phenotypic groups (high and low plasma cholesterol response to the challenge diet). Half of the animals in each group were fed basal diet (8.1% fat and 0.04% cholesterol by weight), and the remainder were fed challenge diet (17.7% fat and 0.61% cholesterol). The plasma cholesterol values of both groups fed the basal diet and of low responders fed the challenge diet were similar. In addition, both very-low-density and low-density lipoproteins (VLDL+LDLs) and high-density lipoproteins (HDLs) were similar among these groups in density and in lipid and apolipoprotein compositions. In contrast, the high responders fed the challenge diet showed a 7-fold increase in total plasma cholesterol, which was primarily a consequence of increases in the VLDL+LDL cholesterol component defined by heparin-Mn precipitation. Moreover, the VLDL+LDLs were more heterogeneous and were characterized by decreased densities. The VLDL+LDLs of the high-responding group had higher levels of apolipoprotein (apo) B and apoE than the other groups. Plasma apoB concentrations estimated by dot blotting techniques increased by 3-fold, and apoE by 44-fold in the high responding group. Understanding the factor(s) mediating responder phenotype in this new model species will expand our knowledge of the regulation of lipemic response to diet.

Dramatically decreased high density lipoprotein cholesterol, increased remnant clearance, and insulin hypersensitivity in apolipoprotein A-II knockout mice suggest a complex role for apolipoprotein A-II in atherosclerosis susceptibility
Weng, W. and J. L. Breslow (1996), Proc Natl Acad Sci U S A 93(25): 14788-94.
Abstract: Apolipoprotein (apo) A-II is the second most abundant apolipoprotein in high density lipoprotein (HDL). To study its role in lipoprotein metabolism and atherosclerosis susceptibility, apo A-II knockout mice were created. Homozygous knockout mice had 67% and 52% reductions in HDL cholesterol levels in the fasted and fed states, respectively, and HDL particle size was reduced. Metabolic turnover studies revealed the HDL decrease to be due to both decreased HDL cholesterol ester and apo A-I transport rate and increased HDL cholesterol ester and apo A-I fractional catabolic rate. The apo A-II deficiency trait was bred onto the atherosclerosis-prone apo E-deficient background, which resulted in a surprising 66% decrease in cholesterol levels due primarily to decreased atherogenic lipoprotein remnant particles. Metabolic turnover studies indicated increased remnant clearance in the absence of apo A-II. Finally, apo A-II deficiency was associated with lower free fatty acid, glucose, and insulin levels, suggesting an insulin hypersensitivity state. In summary, apo A-II plays a complex role in lipoprotein metabolism, with some antiatherogenic properties such as the maintenance of a stable HDL pool, and other proatherogenic properties such as decreasing clearance of atherogenic lipoprotein remnants and promotion of insulin resistance.

Drano for the heart. An experimental drug no one expected to work is surprisingly effective at rooting out cholesterol
Lemonick, M. D. (2003), Time 162(20): 60.

Dried green leaf powders of Jew's mellow (Corchorus), persimmon (Diosphyros kaki) and sweet potato (Ipomoea batatas poir) lower hepatic cholesterol concentration and increase fecal bile acid excretion in rats fed a cholesterol-free diet
Innami, S., K. Tabata, et al. (1998), Plant Foods Hum Nutr 52(1): 55-65.
Abstract: A cholesterol-free diet containing dried powder of Jew's mellow leaves, persimmon leaves or sweet potato leaves respectively at 5% level as dietary fiber was fed to male Sprague-Dawley rats for about one month. The experiment was conducted twice except for sweet potato leaves. In the groups fed the diet mixed with powders of any of the three different dried green leaves, the hepatic cholesterol concentration significantly decreased. Such lowering was not observed in serum cholesterol concentration compared with the control (cellulose) group. A significant increase in fecal weight was observed in all the groups fed the green leaf samples. All the dried green leaves increased fecal excretion of bile acids per gram or per day compared with the control group in both experiments, but only the dried Jew's mellow leaves showed an increased excretion of neutral sterols. These results suggest that lowering of hepatic cholesterol by powdered green leaves is not necessarily due to the same factor, but to the increased fecal excretion of bile acids due to inhibited enterohepatic circulation in animals given these samples.

Dropping cholesterol--safely
Service, R. F. (1994), Science 266(5189): 1323.

Drug and alcohol abuse and cholesterol levels
Gross, G. A. (1994), J Am Osteopath Assoc 94(1): 55-6, 61-2.
Abstract: An uncontrolled, retrospective study of 58 consecutive patients admitted to a hospital substance abuse unit assessed the effects of alcohol consumption on cholesterol levels. From the dietary histories completed by 54 of the patients, it was found that the alcoholics consumed a high-calorie diet containing a high percentage of foods with a high cholesterol content, but in small quantities. Most of their caloric intake was derived from the alcohol. Abusers of substances other than alcohol had a low-calorie intake of the same quality as alcoholics. It appears that low consumption of alcohol rather than something intrinsic in alcohol or other drugs is related to low levels of total cholesterol in persons consuming a high cholesterol-containing diet. The author also suggests that an unexplained relationship between low cholesterol levels and some gastrointestinal malignancies may be due to the effects of alcohol on the gastrointestinal tract.

Drug clinics. How I treat a patient with a low concentration of HDL cholesterol
Scheen, A. J. (1998), Rev Med Liege 53(12): 727-31.
Abstract: The decision to treat an individual with low HDL cholesterol level depends on his overall cardiovascular risk profile and the therapeutic strategy is based upon the characteristics of the lipid profile (isolated abnormality, associated hypertriglyceridaemia or combined elevation of LDL cholesterol). The treatment must favour diet and exercise, before considering a possible pharmacological approach. Results are usually acceptable with better life habits and appropriate diet when low HDL cholesterol level is associated to hypertriglyceridaemia. From a pharmacological point of view, the best results are obtained with fibrates or nicotinic acid. However, results are often disappointing when low HDL cholesterol level is isolated.

Drug control of reverse cholesterol transport
Franceschini, G., J. P. Werba, et al. (1994), Pharmacol Ther 61(3): 289-324.
Abstract: Reverse cholesterol transport identifies a series of metabolic events resulting in the transport of excess cholesterol from peripheral tissues to the liver. 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 may hold promise in the prevention and treatment of arterial disease. Among the agents affecting lipoprotein metabolism, only probucol exerts significant effects on reverse cholesterol transport, by stimulating the activity of the cholesteryl ester transfer protein and, consequently, altering HDL subfraction composition/distribution. Another approach to the stimulation of reverse cholesterol transport consists of raising plasma HDL levels; studies in animals, either by exogenous supplementation or by endogenous overexpression, have shown a consistent benefit in terms of atherosclerosis regression and/or non-progression. Thus, it is time to consider different future treatments of atherosclerosis, combining the classical lipid-lowering treatments with innovative methods to promote cholesterol removal from the arterial wall.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles