| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Children and cholesterol: potential prevention for future good health Snetselaar, L. G. and R. M. Lauer (1991), Bol Asoc Med P R 83(11): 505-7. Abstract: The prevention of cardiovascular disease beginning in childhood may be affected with two strategies. The first is a population approach to lower the cholesterol levels in all American children. The second is an individualized strategy to identify and treat children at particularly high risk in the health care system. |
| Children and cholesterol: what is a physician to do? Marino, R. V. (1991), J Am Osteopath Assoc 91(7): 667-8. |
| Chinese green tea lowers cholesterol level through an increase in fecal lipid excretion Yang, T. T. and M. W. Koo (2000), Life Sci 66(5): 411-23. Abstract: Lung Chen Tea, a Chinese green tea, has been found to lower serum and liver cholesterol. In this study, its dose response and mechanisms of action on cholesterol lowering in diet-induced hypercholesterolemic Sprague-Dawley rats were investigated. The activities of three major lipid metabolizing enzymes, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-Co A) reductase, cholesterol 7alpha-hydroxylase and fatty acid synthase (FAS), as well as fecal excretion of bile acids and cholesterol were examined. Lung Chen Tea administration for eight weeks significantly lowered the serum cholesterol in the 2% and 4% groups. The activities of the three enzymes were not affected by Lung Chen Tea, but the fecal bile acids and cholesterol excretions were significantly increased. These results demonstrated that Lung Chen Tea lowered plasma cholesterol by increasing fecal bile acids and cholesterol excretion. Further investigation is required to evaluate the exact mechanisms of action of Lung Chen Tea. |
| Chinese hamster ovary cell mutants affecting cholesterol metabolism Chang, T. Y., M. T. Hasan, et al. (1997), Curr Opin Lipidol 8(2): 65-71. Abstract: The approach of somatic cell and molecular genetics for the study of intracellular regulation of cholesterol metabolism has blossomed in recent years. This review lists all the Chinese hamster ovary cell mutants involved in cholesterol metabolism. In addition, it summarizes the characteristics of mutants involved in three different processes: (1) sequential cleavage of the membrane-bound sterol regulatory element-binding proteins; (2) cholesterol esterification; and (3) intracellular cholesterol transport from the lysosome/endosome. |
| Chitosan decreases total cholesterol in women: a randomized, double-blind, placebo-controlled trial Bokura, H. and S. Kobayashi (2003), Eur J Clin Nutr 57(5): 721-5. Abstract: BACKGROUND: Hypercholesterolemia is an important risk factor for cardiovascular disease. Orally administered chitosan binds lipids in the small intestine and reduces their absorption. Chitosan has been shown to decrease serum cholesterol in animal and human studies. This study investigated the effectiveness of chitosan in reducing serum cholesterol without concomitant diet therapy. METHODS: Ninety female volunteers (age 34-70 y) with confirmed mild to moderate hypercholesterolemia were enrolled into the study. They were randomly assigned to receive chitosan (1.2 g per day) or placebo in a double-blind manner. Serum lipids, body weight and adverse events were assessed at baseline and after 28 and 56 days of treatment. Subjects maintained their usual diet and documented the type and gross amount of food consumed. RESULTS: Eighty-four subjects (41 chitosan, 43 placebo) were included in the analysis. Chitosan significantly (F=3.19, P=0.04) reduced total cholesterol compared to placebo. In a subgroup of subjects with over 60 y of age, chitosan group significantly reduced total and LDL cholesterol (F=4.21, P=0.02, and F=3.46, P=0.04, respectively) compared with placebo. Adverse effects were few; no serious events were reported. CONCLUSION: Our results demonstrate that chitosan is safe and effective for lowering cholesterol. However, the effect of chitosan for decreasing cholesterol is mild. |
| Chlordecone pretreatment alters 14Cchlordecone and 14Ccholesterol transport kinetics in the perfused rat liver Gilroy, D. J., H. M. Carpenter, et al. (1994), Fundam Appl Toxicol 22(2): 286-92. Abstract: Previous work demonstrated that pretreatment of mice with low doses of the organochlorine insecticide chlordecone (CD) altered the tissue disposition of a subsequent 14CCD or 14Ccholesterol challenge dose. The profile of these changes was consistent with the induction of a protein integral to hepatic CD/cholesterol turnover. The present study was undertaken to confirm similar in vivo effects in the rat and to analyze potential CD-induced changes in hepatic transport kinetics in the perfused rat liver. For in vivo experiments, male, Sprague-Dawley rats were treated with CD (5, 15, or 40 mg/kg) and challenged 3 or 7 days later with a 5 mg/kg 14CCD tracer dose. Rats challenged 3 days after treatment and evaluated 16 hr later showed a dose-dependent decrease in hepatic 14CCD relative to controls. This decrease could not be attributed to alterations in liver mass or total liver lipid. For kinetics studies, rats received 15 mg/kg CD and livers were perfused 3 days later. Following a brief (5-7 min) single-pass perfusion, the perfusate was replaced with recirculating buffer containing albumin-bound 3Holeic acid or high-density lipoprotein-bound 14CCD or 14Ccholesterol. Livers from pretreated animals had significantly decreased rates of 14CCD and 14Ccholesterol uptake. Efflux of 14CCD and biliary excretion of 14Ccholesterol were increased. No changes were observed in uptake or biliary excretion of 3Holeic acid. SDS-PAGE of hepatic cytosol revealed an enhanced band intensity corresponding to a M(r) of 25,600 in livers from pretreated rats.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Chlorination of cholesterol in cell membranes by hypochlorous acid Carr, A. C., J. J. van den Berg, et al. (1996), Arch Biochem Biophys 332(1): 63-9. Abstract: Neutrophils and monocytes produce the highly cytotoxic hypochlorous acid (HOCl) via the myeloperoxidase (MPO)-catalyzed reaction of H2O2 with Cl-. We have investigated the reaction of reagent and MPO-derived HOCl with cholesterol in a purified liposome system, as well as progressively more complex biological systems. The products were identified by thin-layer chromatography (TLC) and characterized by mass spectrometry (MS). TLC of the HOCl-treated samples gave four major cholesterol products with color development typical of oxysterols. Two of the products coeluted with authentic alpha- and beta-chlorohydrin standards. As was the case with the standards, they were readily converted into their respective epoxides during analysis by MS. Gas chromatography-mass spectrometry analysis of the other major product (band 3) gave peaks consistent with epoxides as well as a lateeluting peak with a distinct mass spectrum. Electrospray MS of this product confirmed its identity as a chlorohydrin based on the presence of the predicted molecular ion and 3:1 Cl isotope ratios. Lipids extracted from red cells and isolated red cell membranes were exposed to HOCl and gave identical products to the purified cholesterol liposome system as determined by TLC and MS. Higher concentrations of HOCl were required due to competition by other unsaturated lipids and protein molecules. When intact red cells, neutrophils, and MCF7 mammary carcinoma cells were exposed to HOCl, cholesterol chlorohydrins were formed, as detected by TLC. The formation of cholesterol chlorohydrins could be potentially disruptive to cell membranes and result in cell lysis and death. They could also be potential biomarkers for oxidative damage associated with neutrophil/monocyte activation. |
| Chlorination, water hardness and serum cholesterol in forty-six Wisconsin communities Zeighami, E. A., A. P. Watson, et al. (1990), Int J Epidemiol 19(1): 49-58. Abstract: The Wisconsin Heart Health Research Program measured serum lipids and other clinical parameters among residents of 46 neighbouring small communities in central Wisconsin. The purpose of the study was to determine whether distribution of serum lipids, blood pressure or thyroid hormones differed according to the chlorination of water supply, or to its calcium and magnesium content (hardness). This report examines serum lipid levels in relation to the drinking water characteristics chlorination and hardness. Variables measured on individuals included age, education level, alcohol intake, cigarette smoking, dietary fat and dietary calcium. An analysis of covariance was used to estimate effects of chlorination and hardness on each of the serum lipids, with individual variables included as covariates. Among females, serum cholesterol (SC) levels are significantly higher in chlorinated communities than in non-chlorinated communities. Community SC levels are also higher for males in chlorinated communities, on the average, but differences are smaller and not statistically significant. Low density lipoprotein (LDL) cholesterol levels follow a similar pattern to that for total SC levels, higher in chlorinated communities for females, but not different for males. On the other hand, high density lipoprotein (HDL) cholesterol community means are nearly identical in the chlorinated and non-chlorinated communities for each sex. |
| Chlorthalidone attenuates the reduction in total cholesterol and small, dense LDL cholesterol subclass associated with weight loss Bradley, K., J. M. Flack, et al. (1993), Am J Hypertens 6(7 Pt 1): 636-9. Abstract: Thiazide diuretics are known to raise total and LDL cholesterol. To assess whether chlorthalidone affected levels of putatively atherogenic small, dense LDL (LDL 3), we conducted a 12 week double blind randomized, placebo controlled clinical trial in 34 nonsmoking men aged 35 to 57 years with mild hypertension (DBP 90 to 104 mm Hg). Our a priori hypothesis that chlorthalidone raised LDL 3 levels was not confirmed. However, the fall in LDL 3 (P =.03) and total cholesterol (P =.08) associated with weight loss was attenuated by chlorthalidone. Since weight loss is commonly prescribed during the clinical management of hypertensives with concomitant hypercholesterolemia, consideration should be given to the attenuating effect of chlorthalidone on cholesterol reduction in the management of these patients. |
| Choice of cost-effectiveness measure in the economic evaluation of cholesterol-modifying pharmacotherapy. An illustrative example focusing on the primary prevention of coronary heart disease in Canada Morris, S. and E. Godber (1999), Pharmacoeconomics 16(2): 193-205. Abstract: OBJECTIVE: To evaluate the effect of using different cost-effectiveness measures in the economic evaluation of cholesterol-modifying pharmacotherapy. DESIGN AND SETTING: An economic model was used to examine the extent to which the relative cost effectiveness of cholesterol-modifying agents varies depending upon the cost-effectiveness measure used. The perspective taken was that of the Canadian public healthcare system. PATIENTS: Individuals without coronary heart disease (CHD) with low-density lipoprotein cholesterol (LDL-C) levels in excess of 190 mg/dl. INTERVENTIONS: Cholesterol-modifying pharmacotherapies available in Canada. MAIN OUTCOME MEASURES AND RESULTS: Cost per 1% reduction in LDL-C level; incremental cost per life-year gained; least-cost agent achieving the LDL-C reduction required to meet the target level of 160 mg/dl; incremental cost per life-year gained of agents reaching the target LDL-C level of 160 mg/dl relative to no therapy; incremental cost per life-year gained of agents achieving the target LDL-C level of 160 mg/dl relative to the least-cost agent reaching the target. Each cost-effectiveness measure had a different informational content to decision-makers, both in terms of the usefulness of the information they provided, and in terms of the extent to which they showed one agent to be more cost effective than another. The most cost-effective treatment regimens were fluvastatin 20 mg per day, fluvastatin 40 mg per day, atorvastatin 10 mg per day and atorvastatin 20 mg per day, depending on the pretreatment LDL-C level and the cost-effectiveness measure used. CONCLUSIONS: We recommend that the cost effectiveness of cholesterol-modifying pharmacotherapy be measured using incremental cost per life-year gained in reaching a predefined target LDL-C level. |
| Cholecystectomy prevents expansion of the bile acid pool and inhibition of cholesterol 7alpha-hydroxylase in rabbits fed cholesterol Xu, G., G. Salen, et al. (2001), J Lipid Res 42(9): 1438-43. Abstract: To study the effect of cholecystectomy on the regulation of classic and alternative bile acid syntheses, gallbladder-intact (n = 20) and cholecystectomized (n = 20) New Zealand White rabbits were fed either chow or chow with 2% cholesterol (3 g/day). After 10 days, bile fistulas were constructed in half of each rabbit group to recover and measure the bile acid pool and biliary bile acid flux. After cholesterol feeding, the bile acid pool size increased from 268 +/- 55 to 444 +/- 77 mg (P < 0.01) with a 2-fold rise in the biliary bile acid flux in intact rabbits but did not expand the bile acid pool (270 +/- 77 vs. 276 +/- 62 mg), nor did the biliary bile acid flux increase in cholecystectomized rabbits. Ileal apical sodium-dependent bile acid transporter protein increased 46% from 93 +/- 6 to 136 +/- 23 units/mg (P < 0.01) in the intact rabbits but did not change in cholecystectomized rabbits (104 +/- 14 vs. 99 +/- 19 units/mg) after cholesterol feeding. Cholesterol 7alpha-hydroxylase activity was inhibited 59% (P < 0.001) while cholesterol 27-hydroxylase activity rose 83% (P < 0.05) after cholesterol feeding in the intact rabbits but neither enzyme activity changed significantly in cholesterol-fed cholecystectomized rabbits. Fecal bile acid outputs reflecting bile acid synthesis increased significantly in the intact but not in the cholecystectomized rabbits fed cholesterol.Removal of the gallbladder prevented expansion of the bile acid pool after cholesterol feeding as seen in intact rabbits because ileal bile acid transport did not increase. As a result, cholesterol 7alpha-hydroxylase was not inhibited. |
| Cholelithiasis induced in the Syrian hamster: evidence for an intramucinous nucleating process and down regulation of cholesterol 7 alpha-hydroxylase (CYP7) gene by medroxyprogesterone Gilloteaux, J., S. Karkare, et al. (1997), Microsc Res Tech 39(1): 56-70. Abstract: This report reviews previously published studies from our laboratory and shows some recent morphological data obtained with scanning and transmission electron microscopy regarding gallstone formation and alteration of the gallbladder epithelium in the Syrian hamster model. Both male and female hamsters were treated with female sex steroids (estradiol alone, estradiol and medroxyprogesterone, medroxyprogesterone alone) during one month. The results show that the Syrian hamster is a good model to study bile changes, gallbladder structure changes, including gallstone formation, and the regulation of cholesterol metabolism at the molecular level. Arguments in favor of this animal model are presented and, during gallstone formation, epithelial cell changes, anionic mucus secretion, and formation of gallbladder luminal deposits can be demonstrated. Recent molecular biology observations related to the effect of female sex steroids on liver cholesterol 7 alpha-hydroxylase (CYP7) gene suggest that progestin alone or primed by estrogen down regulates CYP7 transcription and activity. In addition, progesterone in cell culture systems has been shown to enhance intracellular accumulation of free cholesterol by increasing its uptake and synthesis and by decreasing its esterification by inhibiting the activity of acylcoenzyme A: cholesterol acyltransferase. Non-esterified cholesterol is free to migrate to the extracellular spaces and may contribute to nucleation within the bile. It is suggested that these effects of progesterone on cholesterol metabolism combined with the CYP7 gene down regulation, physical changes in the mucus and the hypomotility of the gallbladder and biliary ducts result in hypersaturation of cholesterol in the bile which favors gallstone formation. |
| Cholest-3,5-dien-7-one formation in peroxidized human plasma as an indicator of lipoprotein cholesterol peroxidation potential Hahn, M., M. Tang, et al. (1995), Biochim Biophys Acta 1255(3): 341-3. Abstract: Lipoprotein peroxidation susceptibility is routinely evaluated using products of unsaturated fatty acids as markers (e.g., malonaldehyde). The significance and factors influencing peroxidation of cholesterol moiety of lipoproteins are relatively unknown due to lack of a reliable marker product which can be measured easily. Under the influence of Cu2+ ions, the major product of lipoprotein cholesterol peroxidation (isolated after saponification) was cholest-3-5-dien-7-one (CSD). Apart from gas-liquid chromatography, this compound lends itself for measurement by alternative methods. Due to lack of the 3 beta-hydroxyl group, CSD was separated from the rest of the oxysterols and cholesterol by passing through digitonin-coated silica-gel G and its concentration was determined by absorption at 283 nm. The recovery of CSD by this method exceeded by 87%. The formation of CSD was also sensitive to vitamin E and therefore could be used as an index of lipoprotein cholesterol susceptibility to peroxidation. |
| Cholesterogenesis, lipogenesis, cholesterol degradation to bile acids, and histopathology of the liver in LA/N-cp obese rats Somanchi, M., P. Ghosh, et al. (1997), Hepatology 25(6): 1451-6. Abstract: Various lipid parameters were determined in lean control and LA/NIH-corpulent (LA/N-cp) rats, a normotensive strain showing metabolic characteristics associated with human Type IV hyperlipidemia. Hepatic and plasma total cholesterol, high density lipoproteins (HDL) cholesterol and triglycerides were significantly higher in the obese group than in the control group. Depending upon whether the data were expressed as per gram tissue or per organ, the rates of de novo fatty acid synthesis in the liver and adipose tissue were higher by 61% to 127% (P <.05) and 79% to 355% (P <.05), respectively, in the obese group compared with the lean control group. Similarly, hepatic rate of cholesterol synthesis was higher by 46% to 107% (P <.05) in the obese animals compared with the lean ones. In vivo hepatic rate of HDL2 cholesterol degradation to bile acids was lower in the obese group by 48% to 63% (P <.05). This was confirmed in the perfused liver in spite of the fact that cholesterol uptake from HDL2 was 3- to 4-fold higher in the obese group. These changes in lipid parameters of the obese animals were neither caused by hyperphagia because they were pair-fed with the control group nor caused by increased rate of food consumption because they were meal-fed. At the same time, all these lipid parameters were 17% to 20% higher in ad libitum-fed obese than in pair-fed obese group. Histopathological evaluation of the livers in the obese and control groups also showed prominent lipid droplets in the cytoplasm of the obese liver but not in the lean control liver. Thus, the possible causes of obesity in the LA/N-cp obese rats are higher synthetic rates of lipids coupled with lower rate of degradation of cholesterol to bile acids. |
| Cholesterol & atherosclerosis: a controversy resolved LaRosa, J. C. (1998), Adv Nurse Pract 6(5): 36-7, 39-41. Abstract: We should regard the so-called cholesterol "controversy" as resolved. Elevated cholesterol levels cause coronary disease and probably are an essential ingredient for the development of atherosclerosis. Elevated cholesterol levels should be a cause for concern. From a public health point of view, the ultimate treatment of atherosclerosis will depend on major changes in the lifestyles of populations in developed countries, including a shift to diets that are largely vegetarian, as well as the elimination of tobacco use, an increase in regular exercise, and a reduction in the propensity of to increase weight, particularly with age. For patients at high risk for coronary events, including those with other coronary risk factors and with clinically established coronary disease, cholesterol lowering is absolutely essential. In the majority of cases, it will require not only dietary change but also cholesterol-lowering medication. Taken together, these public health and medical measures can massively reduce, if not eliminate, the burden of atherosclerosis that currently plaques developed countries and now threatens the developing world. |
| Cholesterol (and cardiovascular risk) in adolescence Kohn, M. and M. S. Jacobson (2004), Curr Opin Pediatr 16(4): 357-62. Abstract: PURPOSE OF REVIEW: Atherosclerosis is a significant cause of adult morbidity and mortality. New evidence confirms that it begins in childhood and accelerates at adolescence. Many new studies have solidified the understanding of its risk factors and changed the approach to their clinical management. RECENT FINDINGS: The important descriptions of known risk factors and their clear relation to the pathophysiologic process of atherosclerosis are reviewed here. Some emerging risk factors are discussed. Furthermore, the many new studies on treatment options are reviewed. SUMMARY: These new findings make it imperative that adolescents be screened for traditional risk factors and that they be treated with therapeutic lifestyle change. With the weight of new evidence on the safety and efficacy of statins in this age group, clinicians can feel more confident in their use when indicated. Research into emerging risk factors like obesity, metabolic syndrome, diabetes. and homocysteine will be important in the future management. |
| Cholesterol (thermodynamic) activity determinations in bile salt-lecithin-cholesterol systems and cholesterol-rich liquid crystalline mesophase formation Jain, U. K., W. I. Higuchi, et al. (1992), Pharm Res 9(6): 792-9. Abstract: Previous in vitro studies have shown that tauroursodeoxycholate (TUDC)-lecithin (L) micellar solutions solubilize cholesterol (Ch) poorly compared to its 7 alpha-epimer, taurochenodeoxycholate (TCDC). However, in clinical studies ursodeoxycholic acid (UDC) has been found to be as effective as chenodeoxycholic acid (CDC) in Ch gallstone dissolution, and it has been suggested that, during UDC therapy, liquid crystalline mesophase formation may be involved in enhancing micellar Ch dissolution and dispersion. The purpose of the present study was to investigate whether measurements of the Ch thermodynamic activity (A(T) would provide new insights into the problem of Ch solubilization and mesophase formation in bile salt-lecithin-Ch systems. Using the silicone polymer uptake method developed in this laboratory, A(T) was measured as a function of Ch concentration in the TUDC-L-Ch and TCDC-L-Ch model bile systems. In the TCDC systems Henry's law was obeyed almost up to unit activity (i.e., A(T) was proportional to Ch concentration almost up to A(T) = 1.0). However, in many of the TUDC-containing systems negative deviations from Henry's law were observed well below unit activity and these systems became visibly turbid before saturation with respect to cholesterol monohydrate (ChM) was reached. The effects of varying the TCDC/TUDC ratio upon the A(T) behavior were also studied. With increasing TCDC/TUDC ratio, the onset of mesophase formation was shifted to higher A(T) values. A(T) measurements were also conducted in BS-L-Ch mixtures simulating biles of patients undergoing UDC therapy. The results obtained suggest that mesophase formation may not always occur in biles of patients undergoing UDC therapy.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol Uji, Y. and H. Okabe (1995), Nippon Rinsho 53 Su Pt 1: 615-6. |
| Cholesterol Wootton, J. C. (1999), J Womens Health Gend Based Med 8(4): 555-7. |
| Cholesterol 3-sulfate interferes with cornified envelope assembly by diverting transglutaminase 1 activity from the formation of cross-links and esters to the hydrolysis of glutamine Nemes, Z., M. Demeny, et al. (2000), J Biol Chem 275(4): 2636-46. Abstract: The loss of transglutaminase 1 enzyme (TGase 1) activity causes lamellar ichthyosis. Recessive X-linked ichthyosis (XI) results from accumulation of excess cholesterol 3-sulfate (CSO(4)) in the epidermis but the pathomechanism how elevated epidermal CSO(4) causes ichthyosis is largely unknown. Here we provide evidence that XI is also a consequence of TGase 1 dysfunction. TGase 1 is a key component of barrier formation in keratinocytes: it participates in the cross-linking of cell envelope (CE) structural proteins, and also forms the lipid bound envelope by esterification of long chain omega-hydroxyceramides onto CE proteins. Using involucrin and an epidermal omega-hydroxyceramide analog as substrates, kinetic analyses revealed that at membrane concentrations above 4 mol %, CSO(4) caused a marked and dose-dependent inhibitory effect on isopeptide and ester bond formation. Sequencing of tryptic peptides from TGase 1-reacted involucrin showed a large increase in deamidation of substrate glutamines. We hypothesize that supraphysiological levels of CSO(4) in keratinocyte membranes distort the structure of TGase 1 and facilitate the access of water into its active site causing hydrolysis of substrate glutamine residues. Our findings provide further evidence for the pivotal role of the TGase 1 enzyme in CE formation. |