Cholesterol Journal Articles

Record 6941 to 6960

How common is cholesterol embolism?
Cross, S. S. (1991), J Clin Pathol 44(10): 859-61.
Abstract: Histological sections of spleen and both kidneys from 372 necropsies were examined for the presence of cholesterol emboli. These were identified in nine (2.4%) cases and the clinical histories of these cases were reviewed. All the subjects with cholesterol emboli were older than 60 years and eight out of nine were male. Lesions of differing ages were found in individual cases, suggesting that the process of embolism was recurrent. Two of the cases had undergone arteriography procedures in the month before death and, if these were excluded, then the incidence of "spontaneous" cholesterol embolism was 1.9%. This incidence is much lower than that of previously published studies and may be due to a lower incidence of cholesterol embolism in Britain compared with North America or a decrease in incidence over the past two decades. In three of the subjects with cholesterol embolism the cause of death could be related to systemic atherosclerosis, but in the other six cases there was no apparent correlation between the finding of cholesterol embolism and the cause of death. The clinical relevance of the histological finding of cholesterol embolism can only be assessed in conjunction with clinical information.

How dietary measures can help reduce unhealthy blood cholesterol levels
Cowbrough, K. (2004), Prof Nurse 20(4): 33-5.
Abstract: While cholesterol is produced naturally by our bodies, a high blood concentration of certain types of cholesterol is a predisposing factor for coronary heart disease. Some of the reasons for developing unhealthy levels of cholesterol are discussed, together with some dietary strategies to reduce them to acceptable levels.

How does alcohol raise HDL-cholesterol concentration?
Savolainen, M. J. (1990), Ann Med 22(3): 141-2.

How does the rapid cholesterol tests work?
Schlieper, M. and G. Assmann (1991), Med Monatsschr Pharm 14(12): 372.

How far should one lower LDL cholesterol
Wasielewski, S. (1998), Med Monatsschr Pharm 21(12): 387-90.

How far should the level of LDL cholesterol be decreased?
Giral, P. and G. Turpin (2003), Servir 51(4): 181-6.

How I study a patient with a low concentration of HDL cholesterol
Scheen, A. J. (1998), Rev Med Liege 53(11): 711-4.
Abstract: A decrease in plasma HDL cholesterol concentration is considered as a major cardiovascular risk factor and is a prevalent lipid abnormality among patients with coronary heart disease. This condition is most often observed in the presence of hypertriglyceridaemia, generally linked to the insulin resistance syndrome, but may also be associated to elevated LDL cholesterol level or even be present alone (hypoalphalipoproteinaemia). The decision to treat a patient with low HDL level depends on the individual overall cardiovascular risk which should be evaluated as carefully as possible. The investigation should look for causes which may favour this metabolic condition, such as bad life habits or possible pharmacological interferences.

How is a cholesterol gallstone formed?
Erlinger, S. (1994), Gastroenterol Clin Biol 18(11): 984-7.

How low can you go? New guidelines call for heart patients to cut their cholesterol levels even further
Gorman, C. (2004), Time 164(4): 73.

How much to lower serum cholesterol: is it the wrong question?
Kappagoda, C. T. and E. A. Amsterdam (1999), J Am Coll Cardiol 34(1): 289-92.

How often are Ghananian gallbladder stones cholesterol-rich
Darko, R., E. Q. Archampong, et al. (2000), West Afr J Med 19(1): 64-70.
Abstract: BACKGROUND: Although the prevalence of symptomatic gallbladder stone disease in Ghana increased almost four-fold between 1966 and 1991, little is known about the composition of and aetiopathogenesis of these stones, nor about their suitability for non-surgical (dissolution) treatments. METHODS: To study this, gallstones from 67 out of 90 patients coming to cholecystectomy were retrieved and, based on their external appearance, classified provisionally as cholesterol(chol) (n = 8), black pigment (n = 28) and brown pigment (n = 31) stones. The gallstones were then homogenised, their cholesterol(chol) content measured chemically and the stones re-classified as cholesterol-poor (< 10% chol by weight), intermediate (10-75% chol) and cholesterol-rich (> 75% chol). The relationship between the initial and the definitive classifications was then examined and the biliary bacteriology (carried out on fresh samples of gallbladder(GB) bile obtained by fine needle aspiration) on gallstone composition, analysed. RESULTS: The external appearance correctly predicted stone composition in the 28 thought, initially, to have black pigment stones (all of whom had stones containing < 10% chol by weight, on chemical analysis) and the eight believed, originally to have "cholesterol" stones (all of whom had stones with > 75% chol) but it proved unreliable in the 31 considered, at the time of surgery, to have brown pigment stones (mean chol content 58+ SEM 35%; range 0-98%. By chemical analysis, more than half the patients 35 of 67 or 52% had cholesterol-poor stones, nine (13% of the total) had intermediate stones, while 23 (34%) had cholesterol-rich stones. Cholesterol-rich gallstones were also more frequent in women than in men (p < 0.03). Only nine of 43 patients (21%) whose GB bile was aspirated, had positive bacterial cultures. There was no obvious difference in stone composition between those with positive, and those with negative, cultures. CONCLUSION: Since the majority of Ghanaian patients with cholecystolithiasis have gallbladder stones with < 75% chol by weight, when active treatment is indicated surgery is more appropriate than dissolution therapy. However contrary to common belief, cholesterol-rich gallstones do occur in West Africa: 34% of the present series had stones with > 70% chol by weight.

How reliable is the Reflotron-HDL-cholesterol determination method?
Riesen, W. F. (1990), Schweiz Med Wochenschr 120(51-52): 1971-5.
Abstract: The newly introduced Reflotron-HDL-cholesterol determination was compared with conventional precipitation by phosphotungstate/Mg2+ and quantitation of HDL cholesterol in the supernatant by means of the CHOD PAP method. Accuracy and precision were analyzed by means of three different control materials (Precinorm L, Kontrollogen LP, Reflotron-HDL-Precinorm), which were assessed daily in multiple determinations (n = 10 and 5 respectively) for 5 days. In addition, 100 patient samples, (EDTA plasma) which covered a range from 0.35 to 2.50 mmol/l were compared by both methods. The values of the control sera gave a difference of less than 5% from the target values, and the values from the patients' samples showed less than 3% difference between the two methods. The precision within series was always below 6.5%, and the interassay precision below 3.2%. Reflotron-HDL cholesterol determination appears to meet quality requirements on condition that it is performed by well-trained laboratory personnel.

How should low-density lipoprotein cholesterol concentration be determined?
Faas, F. H., A. Earleywine, et al. (2002), J Fam Pract 51(11): 972-5.
Abstract: The National Cholesterol Education Program Adult Treatment Panel III Report (NCEP-ATP III) has identified low-density lipoprotein cholesterol (LDLC) as the primary target of therapy and has recommended using the Friedewald calculated LDL-C (CLDL- C). The present study compared a direct LDLC (D-LDL-C) method with the C-LDL-C and determined the possible impact on treatment decisions. C-LDL-C and D-LDL-C were compared in 464 consecutive patients. The D-LDL-C was 18% higher than the C-LDL-C at 100 mg/dL, an important level for medical decision making. This can result in inappropriate drug therapy (usually overtreatment) if the NCEP-ATP III treatment guidelines are followed with the D-LDL-C rather than the C-LDL-C. The C-LDL-C is preferred because this assay has been used in clinical trials documenting the benefits of cholesterol-lowering therapy.

How to visualize cholesterol
Shimada, Y. and Y. Ohno-Iwashita (2004), Tanpakushitsu Kakusan Koso 49(10): 1381-7.

How well do we treat elevated LDL-cholesterol? Results from a University Residents' Clinic
Higgins, P. D., C. Russo, et al. (2002), N C Med J 63(5): 247-52.

Human ABCA1 BAC transgenic mice show increased high density lipoprotein cholesterol and ApoAI-dependent efflux stimulated by an internal promoter containing liver X receptor response elements in intron 1
Singaraja, R. R., V. Bocher, et al. (2001), J Biol Chem 276(36): 33969-79.
Abstract: By using BAC transgenic mice, we have shown that increased human ABCA1 protein expression results in a significant increase in cholesterol efflux in different tissues and marked elevation in high density lipoprotein (HDL)-cholesterol levels associated with increases in apoAI and apoAII. Three novel ABCA1 transcripts containing three different transcription initiation sites that utilize sequences in intron 1 have been identified. In BAC transgenic mice there is an increased expression of ABCA1 protein, but the distribution of the ABCA1 product in different cells remains similar to wild type mice. An internal promoter in human intron 1 containing liver X response elements is functional in vivo and directly contributes to regulation of the human ABCA1 gene in multiple tissues and to raised HDL cholesterol, apoAI, and apoAII levels. A highly significant relationship between raised protein levels, increased efflux, and level of HDL elevation is evident. These data provide proof of the principle that increased human ABCA1 efflux activity is associated with an increase in HDL levels in vivo.

Human ABCA7 supports apolipoprotein-mediated release of cellular cholesterol and phospholipid to generate high density lipoprotein
Abe-Dohmae, S., Y. Ikeda, et al. (2004), J Biol Chem 279(1): 604-11.
Abstract: Apolipoprotein-mediated release of cellular cholesterol and phospholipids was induced in HEK293 cells by expressing human ATP-binding cassette transporter A7 (ABCA7) and ABC transporter A1 (ABCA1) proteins, whether transient or stable, to generate cholesterol-rich high density lipoprotein (HDL). Green fluorescent protein (GFP) attached at their C termini did not influence the lipid release reactions. Transfected ABCA7-GFP induced apolipoprotein-mediated assembly of cholesterol-containing HDL also in L929 cells, which otherwise generate only cholesterol-deficient HDL with their endogenous ABCA1. Time-dependent release of cholesterol and phospholipid by apolipoprotein A (apoA)-I was parallel both with ABCA1 and with ABCA7 when highly expressed in HEK293 cells, but dose-dependent profiles of lipid release on apoA-I and apoA-II were somewhat different between ABCA1 and ABCA7. Analyses of the stable clones with ABCA1-GFP (293/2c) and ABCA7-GFP (293/6c) by using the same vector indicated some differences in regulation of their activities by protein kinase modulators. Dibutyryl cyclic AMP increased ABCA1-GFP and the release of cholesterol and phospholipid in 293/2c but increased neither ABCA7-GFP nor the lipid release in 293/6c. Expression of ABCA1-GFP- and apoA-I-mediated lipid release were enhanced in parallel by phorbol 12-myristate 13-acetate (PMA) in 293/2c cells. In contrast, the same treatment of 293/6c increased ABCA7-GFP, but apoA-I-mediated lipid release was significantly suppressed. Despite these different responses to PMA, all of the effects of PMA were reversed by a specific protein kinase C inhibitor Go6976, suggesting that the changes were in fact due to protein kinase C activation. A thiol protease inhibitor, N-acetyl-Leu-Leu-norleucinal, increased the protein levels of ABCA1-GFP in 293/2c and ABCA7-GFP in 293/6c, indicating their common degradation pathway. The data indicated that human ABCA7 would compensate the function of ABCA1 for release of cell cholesterol in a certain condition(s), but post-transcriptional regulation of their activity is different.

Human apoA-I/C-III/A-IV gene cluster transgenic rabbits: effects of a high-cholesterol diet
Recalde, D., N. Baroukh, et al. (2004), FEBS Lett 572(1-3): 294-8.
Abstract: We have generated transgenic rabbits that express the entire human apoA-I/C-III/A-IV gene cluster. As in humans, h-apoA-I and h-apoC-III were expressed in liver and intestine, whereas h-apoA-IV mRNA was detected in intestine only. Transgenic rabbits had significantly higher plasma total cholesterol, HDL-cholesterol and total phospholipid concentrations than non-transgenic littermates. In contrast to similar transgenic mice previously generated, which have gross hypertriglyceridemia, triglyceride concentrations were only moderately raised in transgenic rabbits. Plasma and HDL from transgenic rabbits were more effective than those from controls in promoting cholesterol efflux from cultured hepatoma cells. They had lower LCAT, lower CETP and higher PLTP activities than non-transgenic littermates. Cholesterol-feeding produced major increases in plasma lipids. The qualitative response to the diet was not modified by cluster expression. Human apoA-I concentration was halved by cholesterol-feeding, whereas h-apoC-III and h-apoA-IV concentrations were not significantly altered. Cholesterol efflux from hepatoma cells to plasma and HDL was not altered by the diet. Since lipoprotein metabolism of rabbits closely resembles that of humans, human apoA-I/C-III/A-IV transgenic rabbits may provide a reliable model for studies of the transcriptional regulation of the cluster, and for evaluating the effects of different agents on the expression of the three genes.

Human ApoA-IV overexpression in transgenic mice induces cAMP-stimulated cholesterol efflux from J774 macrophages to whole serum
Fournier, N., V. Atger, et al. (2000), Arterioscler Thromb Vasc Biol 20(5): 1283-92.
Abstract: The role of apolipoprotein A-IV (apoA-IV) in lipoprotein metabolism has not been established. The aim of the present study was to investigate the role of apoA-IV in reverse cholesterol transport by comparing cellular cholesterol efflux to serum or serum fractions from control mice and from mice transgenic for human apoA-IV (HuA-IVTg mice). When Fu5AH hepatoma cells were used, the cholesterol efflux to serum from either control or transgenic mice was similar. When control J774 macrophage cells were used, a comparison of efflux to serum or lipoprotein-deficient serum (LPDS) failed to demonstrate any differences between control and transgenic mice. In contrast, when the J774 cells were pretreated with cAMP, there was a stimulation of efflux to whole serum or LPDS from HuA-IVTg mice. cAMP treatment had no effect on efflux to serum or LPDS from control mice. Pretreatment of the cells with cAMP did not enhance the efflux response to high density lipoprotein isolated from HuA-IVTg mouse serum. Our results suggest that apoA-IV, unassociated with high density lipoprotein particles, is responsible for enhanced cholesterol efflux. This study illustrates the role of lipid-free apolipoproteins in mediating cellular cholesterol efflux with use of a biological fluid and is potentially of physiological relevance, especially in apolipoprotein-rich extravascular fluids.

Human apolipoprotein A-I gene promoter mutation influences plasma low density lipoprotein cholesterol response to dietary fat saturation
Mata, P., J. Lopez-Miranda, et al. (1998), Atherosclerosis 137(2): 367-76.
Abstract: Previous studies have shown that the A to G transition occurring at position -75 bp upstream of the transcriptional start site in the human apolipoprotein A-I gene may affect plasma high density lipoprotein cholesterol (HDL-C) levels and low density lipoprotein cholesterol (LDL-C) response to changes in amount of dietary fat. We have examined the response to dietary fat saturation as a function of this mutation in 50 men and women. Subjects were first fed a saturated (SAT) fat diet (35% fat, 17% SAT) for 28 days, followed by a diet rich in monounsaturated fatty (MUFA) acids (35% fat, 22% MUFA) for 35 days and a diet rich in polyunsaturated (PUFA) fat (35% fat, 13% PUFA) for 35 days. All meals were prepared and consumed at the study sites. Lipoproteins were measured at the end of each diet period. The allele frequency for the A allele was 0.13. Subjects carrying the A allele had higher plasma cholesterol, LDL-C and triglyceride levels than those homozygotes for the G allele. As compared to the SAT diet, a PUFA diet induced significantly greater plasma total (P = 0.003) and LDL-C decreases (P = 0.001) in G/A women (-1.62 and -1.32 mmol/l, respectively) than in G/G subjects (-0.87 and -0.74 mmol/l for plasma and LDL-C, respectively). Multiple regression analysis demonstrated that in women, the variability in LDL-C response from a diet rich in SAT fat to a diet rich in PUFA was primarily due to LDL-C levels (during the SAT phase), accounting for 55.1% of the variance, waist to hip ratio (W/H; 11.4%) and the G/A polymorphism (10%). Whereas in men the major determinant of this response was smoking (21.4%). In conclusion, the G/A polymorphism appears to have a small but significant effect on plasma LDL-C responsiveness to changes in dietary fat saturation specially in women.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles