Cholesterol Journal Articles

Record 4521 to 4540

DNA polymorphisms of the apolipoprotein B and A-I/C-III genes are associated with variations of serum low density lipoprotein cholesterol level in childhood
Aalto-Setala, K., J. Viikari, et al. (1991), J Lipid Res 32(9): 1477-87.
Abstract: A number of restriction fragment length polymorphisms (RFLPs) of the apolipoprotein B (apoB) and apolipoprotein A-I/C-III(apoA-I/C-III) genes have been found to be associated with serum lipoprotein levels in many adult populations. In order to examine whether these genetic polymorphisms influence serum lipoprotein levels in childhood and adolescence, we determined the apoB XbaI and apoA-I/C-III SstI genotypes and serum lipoprotein concentrations in 307 healthy Finns aged 9 to 21 years. In the age groups of 9, 12, and 15 years, subjects homozygous for the X2 allele (the XbaI site present) of the apoB gene had mean serum low-density lipoprotein (LDL) cholesterol levels (3.69, 3.43, and 3.15 mmol/l, respectively) that were 12-20% higher than those in subjects homozygous for the absence of this allele (3.08, 3.02, and 2.80 mmol/l, respectively). This association was more significant in males than in females. At the age of 9 to 18 years, subjects carrying the S2 allele (SstI site present) of the apoA-I/C-III gene complex had an approximately 6-15% higher mean serum LDL-cholesterol level than those homozygous for its absence. The combined genotype X2+S2+ (the simultaneous presence of the X2 allele and the S2 allele) was associated with an even more marked elevation of serum LDL-cholesterol level than either allele alone. As an example, the serum LDL cholesterol concentration was 20% higher in 9-year-old subjects with at least one X2 and one S2 allele than in those without either allele (3.55 vs. 2.97 mmol/l, P less than 0.005). The S2 allele was found to be significantly more frequent in eastern than in western Finland, whereas no significant areal differences were seen in the occurrence of the X2 allele. In conclusion, genetic variations of the apoB and apoA-I/C-III gene loci influence serum lipoprotein concentrations already in childhood.

Do arterial effects of antihypertensive drugs depend on subject's serum cholesterol?
Megnien, J. L., A. Simon, et al. (2001), J Cardiovasc Pharmacol 38(4): 520-8.
Abstract: Effects of antihypertensive treatment on large arteries may be influenced by the type of drug and concomitant risk factors such as blood cholesterol. To explore these possibilities we investigated the common carotid artery of 20 subjects with low cholesterol and 19 subjects with high cholesterol, all with essential hypertension, randomly allocated to 3 months of treatment with nitrendipine (20 mg/d) or trandolapril (2 mg/d). Carotid parameters were determined by recording instantaneous pressure (applanation tonometry) and diameter (echotracking device) and by modeling the pressure-diameter loop to obtain the Peterson modulus, stiffness index, measured and isobaric compliances, and wall viscosity. Effects of drugs on carotid parameters did not differ, except on systolic and diastolic diameters (p < 0.01), which increased insignificantly under nitrendipine but decreased (p < 0.01) under trandolapril. Blood cholesterol status did not influence carotid effects of trandolapril, whereas patients with low and high cholesterol treated with nitrendipine exhibited significant differences in drug effects on (a) systolic and pulse pressures (p < 0.05), which decreased in patients with low cholesterol (p < 0.01, p < 0.05) but not in those with high cholesterol; (b) diastolic diameter (p = 0.05), which increased insignificantly in patients with low cholesterol but was unchanged in those with high cholesterol; and (c) wall viscosity (p < 0.01), which decreased in patients with low cholesterol (p < 0.05) but increased insignificantly in those with high cholesterol. Also, wall viscosity change under nitrendipine was positively related to the baseline blood cholesterol (r = 0.64, p < 0.01). Thus, nitrendipine and trandolapril show noteworthy differences in their effects on the carotid artery, in particular with respect to the status of blood cholesterol, but these differences should be confirmed by larger studies.

Do cholesterol-lowering agents affect brain activity? A comparison of simvastatin, pravastatin, and placebo in healthy volunteers
Harrison, R. W. and C. H. Ashton (1994), Br J Clin Pharmacol 37(3): 231-6.
Abstract: 1. The effects of simvastatin and pravastatin on measures of central nervous system activity were investigated in a double-blind, placebo-controlled, randomised crossover study. 2. Twenty-five healthy volunteers sequentially took 40 mg day-1 simvastatin, 40 mg day-1 pravastatin or placebo for 4 weeks, separated by a 4-6 week washout phase. 3. CNS measures included EEG evoked potentials, power spectral analysis, Leeds Sleep Questionnaire, Hospital Anxiety Depression (HAD) Scale, and Digit Symbol Substitution Test (DSST); biochemical measures included plasma cholesterol, liver enzymes (gamma-GT, AST, ALT) and creatine kinase. 4. Mean cholesterol concentrations with both drugs were significantly lower than with placebo, and the cholesterol-lowering effect was greater with simvastatin. There were no significant differences between treatment in EEG evoked potentials, HAD Scale, or DSST scores. On the sleep measure, subjects reported significantly greater difficulty in getting to sleep while on simvastatin than on pravastatin, but neither score differed from placebo. No significant correlations were observed between sleep ratings and either plasma cholesterol concentrations or EEG evoked potentials. 5. The study showed that, while both drugs reduced plasma cholesterol concentrations, neither exerted significant effects, compared with placebo, on EEG evoked potentials, mood, sleep, or cognitive performance after 4 weeks of chronic administration in healthy volunteers.

Do DNA sequence variants in ABCA1 contribute to HDL cholesterol levels in the general population?
Pajukanta, P. (2004), J Clin Invest 114(9): 1244-7.
Abstract: HDL has a key role in reverse cholesterol transport, mobilizing cholesterol from the peripheral tissues to liver. In this process, the ABC transporter A1 (ABCA1) protein controls the efflux of intracellular cholesterol to apoAI, the major apolipoprotein of HDL. Since ABCA1 mutations were discovered to cause Tangier disease, a rare recessive HDL deficiency, it has been speculated that sequence variants in ABCA1 might also contribute to variations in plasma HDL cholesterol levels in the general population. A new study provides genetic evidence supporting this hypothesis.

Do healthy adults need to know their cholesterol level?
Weaver, K. D., W. T. t. Smith, et al. (1996), N C Med J 57(5): 275-8.

Do hypertensive patients with average cholesterol levels benefit from atorvastatin therapy?
Hackam, D. G. (2003), Cmaj 168(13): 1689.

Do low cholesterol levels slow mental processing?
Benton, D. (1995), Psychosom Med 57(1): 50-3.
Abstract: The plasma cholesterol levels of 279 students were measured and related to decision and movement times in choice reaction time tasks with one, two, four, and eight lamps. In female subjects, low plasma cholesterol levels were associated with slower movement times and, when responding to one or two lamps, slower decision times. In male subjects, there was a nonlinear relationship between cholesterol level and decision times. Because these data are correlational in nature, it is not possible to assume a causal relationship between cholesterol levels and speed of mental processing. The literature, however, supports the suggestion that further work should consider the possibility of a causal relationship.

Do neonates with high serum cholesterol levels have a different high density lipoprotein composition?
Bastida, S., S. Perea, et al. (1998), Eur J Pediatr 157(1): 66-70.
Abstract: In order to ascertain whether the high density lipoprotein (HDL) composition of neonates with high serum cholesterol levels (> or =2.59 mmol/l or > or =100 mg/dl) differs from that of neonates with normal serum cholesterol levels (< 2.59 mmol/l), 548 cord blood samples were examined from full-term newborns of the Toledo Study (Spain) of whom no perinatal factors were known which could alter cord blood lipid levels. Newborns were selected according to the following criteria: single and eutocic delivery with cephalic presentation, gestational age between the beginning of the 37th week and the end of the 41st week, body weight between 2.5 kg and 3.999 kg and an Apgar score of > or =7 and > or =9 at 1 min and 5 min, respectively. The prevalence of high serum total cholesterol (TC) level was greater (P < 0.02) in females than in males. Newborns with high TC levels had higher triglyceride (P < 0.01), HDL-cholesterol (P < 0.001) and apoprotein (Apo) A-I (P < 0.001) levels, and a higher TC/HDL-cholesterol ratio (P < 0.05), but a lower HDL-cholesterol/Apo A-I ratio (P < 0.05). ANOVA two-way analysis showed a significant effect of gender and serum cholesterol level and a statistical interaction of these two factors upon triglycerides, Apo A-I, and the HDL-cholesterol/Apo A-I ratio. However, HDL-cholesterol and the TC/HDL-cholesterol ratio were higher in neonates (males plus females) with high serum TC but they were not affected by sex. The larger HDL particles in males with high TC levels (HM) should be associated with the higher triglyceride level found in those individuals. CONCLUSION: The composition of high density lipoproteins in newborns is influenced by the serum cholesterol level and by gender. Neonates with high total cholesterol have larger average high density lipoprotein (HDL) particles. If total cholesterol is elevated, HDL from males carries more cholesterol than HDL from females.

Do not allow the commercialization of the cholesterol test in the USA to encourage us to misguided health promotion!
Werko, L. (1990), Lakartidningen 87(20): 1745-6.

Do oxysterols control cholesterol homeostasis?
Bjorkhem, I. (2002), J Clin Invest 110(6): 725-30.

Do proteins facilitate the formation of cholesterol-rich domains?
Epand, R. M. (2004), Biochim Biophys Acta 1666(1-2): 227-38.
Abstract: Both biological and model membranes can exhibit the formation of domains. A brief review of some of the diverse methodologies used to identify the presence of domains in membranes is given. Some of these domains are enriched in cholesterol. The segregation of lipids into cholesterol-rich domains can occur in both pure lipid systems as well as membranes containing peptides and proteins. Peptides and proteins can promote the formation of cholesterol-rich domains not only by preferentially interacting with cholesterol and being sequestered into these regions of the membrane, but also indirectly as a consequence of being excluded from cholesterol-rich domains. The redistribution of components is dictated by the thermodynamics of the system. The formation of domains in a biological membrane is a consequence of all of the intermolecular interactions including those among lipid molecules as well as between lipids and proteins.

Do public cholesterol screenings really screen?
McBride, P. E., J. Leovy, et al. (1991), Fam Pract Res J 11(3): 291-300.
Abstract: Two hospital-sponsored cholesterol-screening programs were evaluated to assess whether they detected individuals with undiagnosed high blood cholesterol. Surveys asking about prior testing, knowledge of cholesterol level, and participant characteristics were examined to test screening utilization. In both screenings 54% of participants reported having prior cholesterol testing, only 56% of whom knew their cholesterol level. Of previously untested participants, 8% had high blood cholesterol levels and 13% had borderline levels. Only 65% of participants with a personal or family history of heart attack were aware of their cholesterol level. To attract individuals without prior testing, screening planners should consider locations (eg, worksites and schools) and methods (eg, weekend screenings) to target underrepresented groups in community-wide cholesterol screenings. We encourage an increased emphasis on individualized exit education for participants, especially those who know their cholesterol level or have multiple risk factors for vascular disease. Physicians planning public screenings can utilize this data to develop parameters for referrals from the screenings.

Do total and high density lipoprotein cholesterol and triglycerides act independently in the prediction of ischemic heart disease? Ten-year follow-up of Caerphilly and Speedwell Cohorts
Yarnell, J. W., C. C. Patterson, et al. (2001), Arterioscler Thromb Vasc Biol 21(8): 1340-5.
Abstract: Several studies have suggested that men with raised plasma triglycerides (TGs) in combination with adverse levels of other lipids may be at special risk of subsequent ischemic heart disease (IHD). We examined the independent and combined effects of plasma lipids at 10 years of follow-up. We measured fasting TGs, total cholesterol (TC), and high density lipoprotein cholesterol (HDLC) in 4362 men (aged 45 to 63 years) from 2 study populations and reexamined them at intervals during a 10-year follow-up. Major IHD events (death from IHD, clinical myocardial infarction, or ECG-defined myocardial infarction) were recorded. Five hundred thirty-three major IHD events occurred. All 3 lipids were strongly and independently predictive of IHD after 10 years of follow-up. Subjects were then divided into 27 groups (ie, 3(3)) by the tertiles of TGs, TC, and HDLC. The number of events observed in each group was compared with that predicted by a logistic regression model, which included terms for the 3 lipids (without interactions) and potential confounding variables. The incidence of IHD was 22.6% in the group with the lipid risk factor combination with the highest expected risk (high TGs, high TC, and low HDLC) and 4.7% in the group with the lowest expected risk (P<0.01). A comparison of the predicted number of events in the 27 groups with the number of events observed showed that a logistic regression provided an adequate fit without the need to incorporate interactions between lipids in the model. Conclusions are as follows: (1) Serum TGs, TC, and HDLC are independently predictive of IHD at 10 years of follow-up. (2) Combinations of adverse levels of the 3 major lipid risk factors have no greater impact on IHD than that expected from their individual contributions in a logistic regression model. There was no evidence that men with low HDL/raised TGs were at significantly greater risk than that predicted from the independent effects of the 2 lipids considered individually.

Do we really have sufficient answers to cholesterol questions?
Berglund, G. (1991), Lakartidningen 88(3): 108, 110.

Do you know your total cholesterol (TC) number?
Chen, C., Z. Zhou, et al. (2002), J Biopharm Stat 12(2): 179-92.
Abstract: Total cholesterol (TC) measurements are subject to errors primarily because of temporal variations in cholesterol levels within each individual. These errors make it difficult to estimate the proportion of study subjects with true (error-free) TC in a specific range, an extremely important parameter to policy makers in health care management. To properly address this issue, it is key to accurately estimate the distribution function of the true TC, which typically deviates from the normal distribution. To better approximate the distribution function of the true TC, we propose a constrained maximum likelihood estimator based on a mixture-of-normals model. A simulation study illustrates that the proposed estimator performs better than an estimator based on the normality assumption that is frequently used in the literature to address the same issue. Finally, the proposed estimator is applied to data from a study, and its performance is once again compared with that of an estimator based on the normality assumption.

Does a HDL injection reduce the development of serum hyperlipidemia and progression of fatty streaks in cholesterol fed rabbits?
Beitz, J., A. Beitz, et al. (1992), Prostaglandins Leukot Essent Fatty Acids 47(2): 149-52.
Abstract: The influences of homologous (rabbit) or heterologous (human) high density lipoprotein (HDL) on the development of serum hyperlipidemia and progression of fatty streaks were studied in cholesterol fed rabbits. Three groups of New Zealand rabbits were fed a 0.5% cholesterol rich diet for 8 weeks. Additionally into these animals the following solutions were injected intravenously two times per week: group 1 (control): saline; group 2: human HDL dissolved in saline; group 3: rabbit HDL dissolved in saline. The animals of group 2 had lower serum cholesterol levels during the dietary period than rabbits of group 1 (p < 0.05) but the surface of intima covered with fatty streaks was the same as in group 1. On the other hand, the serum cholesterol level in rabbits of group 3 was the same as in group 1 during the whole experimental period, but the surface of aorta covered with fatty streaks was significantly lower (p < 0.05) in group 3 than in group 1. The results of this study support the hypothesis of an antiatherogenic action of HDL, which seems to be independent of the influence of HDL on the serum lipids but depends on the source of HDL.

Does a high level of HDL-C cholesterol undo the bad effects of a high LDL-C cholesterol?
Perris, A. L., A. G. Bartel, et al. (1999), N C Med J 60(4): 217-21.

Does a lipid clinic increase compliance with National Cholesterol Education Program Treatment Guidelines? Report of a case-matched controlled study
Yates, S., L. Annis, et al. (2001), South Med J 94(9): 907-9.
Abstract: Despite a national effort to promote measurement of cholesterol levels in adults, previous studies have shown that poor control is the norm. We sought to determine the effects of implementation of a structured lipid treatment program. Forty-one clinic-managed patients were matched with similar control patients. Clinic patients had more risk factors overall and therefore lower low-density lipoprotein (LDL) goals. They had significantly greater LDL reduction after the 6-month visit, resulting in a lower final LDL level. The percentage of patients reaching the LDL goal recommended by the National Cholesterol Education Program (NCEP) was the primary endpoint of the study. The NCEP guidelines were followed more frequently within the clinic, and significantly more clinic patients were treated to NCEP LDL goal than control patients. When indicated, medication was more frequently used and titrated in clinic patients. This study shows the efficacy of an organized lipid treatment clinic in management of dyslipidemia.

Does apolipoprotein E genotype influence dietary modification of circulating cholesterol concentrations?
Jones, P. J. (1998), Am J Clin Nutr 68(6): 1151-2.

Does bile salt-stimulated lipase affect cholesterol uptake when bound to rat intestinal mucosa in vitro?
Falt, H., O. Hernell, et al. (2002), Pediatr Res 52(4): 509-15.
Abstract: Bile salt-stimulated lipase (BSSL), or carboxyl ester lipase, is a constituent of exocrine pancreatic secretion and, in some species, including humans, also of milk. BSSL has been suggested to have a direct effect on intestinal uptake of dietary cholesterol besides being the key enzyme in the hydrolysis of fat-soluble vitamins and cholesterol esters. Furthermore, an intestinal heparin-containing receptor for the enzyme has been implicated. If BSSL promotes dietary cholesterol utilization, this might be of particular importance in the neonatal period, which is characterized by a high need of cholesterol for membrane synthesis. We have studied binding of BSSL to intestinal membranes in vitro and if such binding affects the uptake of cholesterol. BSSL bound avidly to rat intestinal microvesicle membranes and the binding was inhibited by addition of free heparin or heparin fragments. In this model system, we could not demonstrate any effect of BSSL on cellular uptake of free cholesterol. However, if esterified rather than free cholesterol was present in the incubation, hydrolysis by BSSL was the rate-limiting step in cellular cholesterol uptake. We therefore conclude that BSSL is important for utilization of dietary cholesterol only by hydrolyzing cholesterol esters and not by acting as a transport protein.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles