| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol, lipid rafts, and disease Simons, K. and R. Ehehalt (2002), J Clin Invest 110(5): 597-603. |
| Cholesterol, lipoprotein and phospholipid levels in acute lymphoblastic leukaemia Shokumbi, W. A., J. E. Ahaneku, et al. (1991), Eur J Haematol 46(1): 59-61. |
| Cholesterol, macrophages, and gene expression of TGF-beta 1 and fibronectin during nephrosis Ding, G., I. Pesek-Diamond, et al. (1993), Am J Physiol 264(4 Pt 2): F577-84. Abstract: Hypercholesterolemia aggravates experimental progressive glomerular injury. Evidence suggests the infiltrating glomerular macrophage (M phi) is a potential effector mechanism for the noxious effects of hypercholesterolemia. Because transforming growth factor (TGF)-beta 1 is secreted by activated M phi s and also stimulates fibronectin production by glomerular cells, we evaluated the kinetics of gene expression for these moieties in glomeruli isolated from nephrotic rats at 3, 7, 11, and 42 days after the delivery of puromycin aminonucleoside (PA). We also assessed whether cholesterol feeding, which raises the glomerular M phi number, alters the glomerular mRNA levels for TGF-beta 1 and fibronectin. Glomerular mRNA levels for TGF-beta 1 and fibronectin in nephrotic rats exhibited a biphasic temporal pattern, decreasing significantly below control at 3 and 7 days after PA but increasing significantly at 11 and 42 days after PA. The upregulated gene expression for TGF-beta 1 and fibronectin at 11 days after PA temporally corresponded to the phase of mesangial M phi infiltration in this model. Cholesterol feeding to both normal and nephrotic rats significantly increased glomerular TGF-beta 1 and fibronectin mRNA levels at 11 days after PA. Immunohistochemical labeling for M phi s and intracellular TGF-beta 1 demonstrated both mesangial and cortical interstitial localization with the TGF-beta1-positive cells possessing M phi nuclear morphology. These findings identify a novel interaction between hypercholesterolemia, augmented glomerular M phi accumulation, and upregulated glomerular TGF-beta 1 and fibronectin gene expression. These perturbations within the acutely injured glomerulus constitute an early pathobiological determinant for the later development of mesangial matrix expansion and glomerulosclerosis. |
| Cholesterol, omega-3 fatty acids, and suicide risk: empirical evidence and pathophysiological hypotheses Brunner, J., K. G. Parhofer, et al. (2001), Fortschr Neurol Psychiatr 69(10): 460-7. Abstract: Studies in psychiatric patients described an association between lower serum cholesterol concentrations, suicidality, depression, impulsivity, and aggression which is not entirely attributable to depression-related malnutrition and weight-loss. Several lines of evidence suggest that a serotonergic deficit in the prefrontal cortex may predispose vulnerable subjects to impulsive, autoaggressive, and suicidal behaviour in stressful life-events. In-vitro studies, animal experiments, and human in-vivo studies support the hypothesis that cholesterol reduction may contribute to the serotonergic abnormalities which have been postulated in suicidal subjects. Recently it was hypothesized that decreased consumption of polyunsaturated fatty acids, especially omega-3 fatty acids, may be a risk factor for depression and suicide. Data from human studies in healthy volunteers suggest that increasing the dietary intake of omega-3 fatty acids may increase central serotonergic activity and reduce impulsive and aggressive behaviours. Earlier epidemiological studies showed an association between low cholesterol concentrations and increased suicide risk. Recent epidemiological studies with greater samples and longer follow-up periods, however, even showed a positive correlation between cholesterol concentrations and suicide risk after controlling for potential confounding variables. Large trials of statins (simvastatin, lovastatin, pravastatin) did not show an increase of suicide mortality. |
| Cholesterol, oxidative stress, and Alzheimer's disease: expanding the horizons of pathogenesis Pappolla, M. A., M. A. Smith, et al. (2002), Free Radic Biol Med 33(2): 173-81. Abstract: Recent epidemiological, clinical, and experimental data suggest that cholesterol may play a role in Alzheimer's disease (AD). We have recently shown that cholesterolemia has a profound effect in the development and modulation of amyloid pathology in a transgenic model of AD. This review summarizes recent advancements in our understanding of the potential role of cholesterol and the amyloid beta protein in initiating the generation of free radicals and points out their role in a chain of events that causes damage of essential macromolecules in the central nervous system and culminates in neuronal dysfunction and loss. Experimental data links cholesterol and oxidative stress with some neurodegenerative aspects of AD. |
| Cholesterol, phospholipid and phospholipase activity of ampullary and isthmic fluid from the bovine oviduct Grippo, A. A., S. H. Anderson, et al. (1994), J Reprod Fertil 102(1): 87-93. Abstract: Cholesterol and phospholipid concentrations and phospholipase activity were measured in fluid from cannulae collected from the bovine oviductal isthmus and ampulla at different stages of the oestrous cycle. The cholesterol concentration and cholesterol normalized by protein were significantly (P = 0.03) greater in isthmic oviductal fluid (224.3 +/- 42.7 micrograms ml-1 over all stages) than in ampullary oviductal fluid (164.5 +/- 11.3 micrograms ml-1), and maximal concentrations (284.5 +/- 25.5 micrograms ml-1) were found during the luteal stage (serum progesterone concentration > or = 1.5 ng ml-1). The concentrations of the phospholipids sphingomyelin and lysophosphatidylcholine increased at different stages of the cycle and in different regions. In the ampulla, the concentration of sphingomyelin was significantly (P < 0.05) greater in oviductal fluid collected during the luteal phase (12.1 +/- 2.7% of total phospholipids) than in fluid collected near oestrus and ovulation (7.5 +/- 1.5% and 6.9 +/- 1%, respectively). The concentration of lysophosphatidylcholine was greater (P < 0.01) in ampullary (19.2 +/- 1.6% of total phospholipids) than in isthmic oviductal fluid (9.9 +/- 1.1%) collected near ovulation. The ratio of cholesterol to total phospholipid was highest in oviductal fluid collected from the isthmus during all stages (2.3 micrograms ml-1:% total phospholipid), while the minimal ratio was found in ampullary fluid collected near ovulation (1.5). Phospholipase activity was higher (P = 0.03) in isthmic oviductal fluid (20.4 +/- 3.2% product formed) than in ampullary oviductal fluid (14.6 +/- 1.4%); the lowest activity (12.6 +/- 1.7% product formed) was in fluid collected during the phase of the oestrous cycle immediately before ovulation.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol, phospholipid, and protein changes in focal opacities in the human eye lens Duindam, J. J., G. F. Vrensen, et al. (1998), Invest Ophthalmol Vis Sci 39(1): 94-103. Abstract: PURPOSE: Focal opacities are signs of early cataractogenesis in the human lens. They progress slowly over a lifetime and may be precursors of mature cataracts. The authors analyzed changes in proteins, phospholipids, and cholesterol in these opacities using in situ techniques: Raman microspectroscopy, filipin cytochemistry for cholesterol, and transmission electron microscopy (TEM). METHODS: Human lenses with verified focal opacities were fixed in 1% paraformaldehyde. Slabs with opacities were analyzed using confocal Raman spectroscopy, then filipin Raman analysis of cholesterol, and finally TEM. RESULTS: Compared with normal fibers, opacities consistently showed elevated levels of cholesterol and aliphatic chains, increased phospholipid acyl chain disorder, and changes in phospholipid lateral packing. Disulfide bridges of specific geometry (trans-gauche-trans) were found. Although protein content was unchanged, compared with normal fibers, aromatic amino acid content was significantly lower. The hydrophobicity of tyrosine residues showed a significant decrease, and a change in the tryptophan indole ring angle was found. The changes were abrupt and sharply delineated focal opacities. TEM confirmed this sharp boundary and showed that the opacities were densely packed with vesicles of varying size and electron density embedded in a homogenous matrix. CONCLUSIONS: The Raman and TEM analyses of opacities showed that early cataractogenic events led to disruption of fiber membranes, formation of vesicles from the membrane constituents, and protein changes. The aberrant morphology of the membranes enveloping the focal opacities may have segregated the affected fibers from the surrounding normal tissue, thus explaining the stationary or slowly progressing character of these opacities. |
| Cholesterol, phospholipids and markers of the function of the accessory sex glands in the semen of men with hypercholesterolaemia Grizard, G., B. Sion, et al. (1995), Int J Androl 18(3): 151-6. Abstract: The effect of hypercholesterolaemia on the cholesterol and phospholipid content of spermatozoa and seminal plasma was studied. Testosterone and specific markers of the accessory sex glands were also measured. Semen samples from 11 hypercholesterolaemic patients (plasma cholesterol > 6.42 mmol/l, plasma triglycerides < 2 mmol/l) were compared with those of 11 normocholesterolaemic controls (plasma cholesterol < 5.14 mmol/l, plasma triglycerides < 2 mmol/l). Cholesterol, phospholipids and the molar ratio of cholesterol: phospholipids were not significantly different between the two groups of patients either in spermatozoa or in seminal plasma. In hypercholesterolaemic patients the total amount of carnitine in the ejaculate was significantly higher, but there were no significant differences in the levels of acid phosphatase or fructose. There were no significant differences in seminal plasma levels of testosterone in the two groups of subjects. These results suggest that hypercholesterolaemia has no effect on cholesterol and phospholipid levels in spermatozoa and does not cause gross modification of the secretory function of the accessory sex glands. |
| Cholesterol, primary and secondary prevention, and all-cause mortality Criqui, M. H. (1991), Ann Intern Med 115(12): 973-6. Abstract: Clinical trials of cholesterol lowering in apparently healthy persons (primary prevention) and in persons with known coronary disease (secondary prevention) routinely show a decrease in the incidence of nonfatal and fatal coronary events. Primary prevention trials, however, generally have failed to show a beneficial effect of cholesterol lowering on total mortality, because of both low overall death rates and a disturbingly high number of deaths from noncoronary causes in the treatment groups. Studies of secondary prevention give more clear-cut evidence of benefit. The rate of death from coronary heart disease is extremely high in these studies, overwhelming the rates for other causes of death. Thus, a possible increase in noncoronary deaths is of much less concern in secondary prevention studies. A possible link between cholesterol lowering and noncoronary causes of death should be explored using dose-response analyses of existing data sets, in both individual studies and aggregate meta-analysis; such analyses should be similar to those that have been done to study the relation between cholesterol lowering and coronary events. These analyses would greatly assist us in developing safe, efficacious ways to prevent coronary heart disease. |
| Cholesterol, racial variation and targeted medicines Topol, E. J. (2005), Nat Med 11(2): 122-3. |
| Cholesterol, serotonin, and behavior in young monkeys Fontenot, M. B., J. R. Kaplan, et al. (1996), Ann N Y Acad Sci 794: 352-4. |
| Cholesterol, statins and dementia Wolozin, B. (2004), Curr Opin Lipidol 15(6): 667-72. Abstract: PURPOSE OF REVIEW: Advances in cholesterol biology suggest that cholesterol metabolism modulates beta-amyloid production, and that pharmaceuticals that inhibit cholesterol metabolism might be valuable in therapy of Alzheimer's disease. Although the genetics and cell biology continue to support the link between cholesterol and Alzheimer's disease, recent clinical studies suggest that the animal studies might not directly translate to clinical studies in humans. RECENT FINDINGS: This review will highlight advances in genetics, cell biology and clinical sciences investigating the relationship between cholesterol and Alzheimer's disease. SUMMARY: Cholesterol, its catabolites and proteins that regulate cholesterol levels all modulate processing of amyloid precursor protein. Statins hold promise in therapy of Alzheimer's disease, but the current data are more consistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-amyloid production. |
| Cholesterol, stroke risk, and stroke prevention Ansell, B. J. (2000), Curr Atheroscler Rep 2(2): 92-6. Abstract: Serum cholesterol traditionally has been considered a poor predictor of total stroke risk; however, it is associated positively with ischemic stroke risk and associated negatively with hemorrhagic stroke risk. Although studies failed to demonstrate stroke reduction using older cholesterol-lowering medications, recent study of the statin class of medications shows both consistent stroke and other cardiovascular benefits. Ischemic stroke and coronary heart disease share similar underlying mechanisms, likely explaining much of the therapeutic benefit from statins. Current research is directed at further determining groups of patients most likely to benefit from lipid reduction in stroke prevention. In the interim, patients with established atherosclerosis should be treated with a statin to achieve a low-density lipoprotein cholesterol level less than 100 mg/dL. |
| Cholesterol, synaptic function and Alzheimer's disease Koudinov, A. R. and N. V. Koudinova (2003), Pharmacopsychiatry 36 Suppl 2: S107-12. Abstract: We experimentally modeled neuronal cholesterol imbalance by creating an acute biochemical increase in cholesterol turnover in rat hippocampal slices. This kind of experimental set-up impairs the redistribution of cholesterol from one cell to another via lipoprotein transport. While increasing cholesterol removal or immediately afterwards, we evoked and recorded two brain waveforms, paired pulse facilitation (PPF) and long-term potentiation (LTP), which indicate neurotransmission and synaptic plasticity, respectively. We found that the lack of cholesterol supply to neurons impaired both PPF and LTP. From additional immunofluorescent analysis of the slices, we could demonstrate that the cholesterol imbalance also caused neurodegeneration of hippocampal neural cell processes and the appearance of tau protein pathology in the mossy fibers. We also analyzed rats fed a cholesterol diet and discovered that they had increased hippocampal cholesterol biosynthesis and impaired LTP. Cholesterol-fed rats were also characterized by Alzheimer's-like brain amyloid that we did not observe in the model of acute cholesterol imbalance. Our data and research by others suggest that biological cholesterol homeostasis dysregulation itself plays a key role in synaptic plasticity impairment and neuronal degeneration, and is the primary cause for several Alzheimer's disease hallmarks not limited to brain amyloids. Moreover, changes in the neurochemistry of amyloid beta, tau, neuronal cytoskeleton, and oxidative stress reactions due to Alzheimer's likely represent physiological transitory mechanisms that aim to compensate impaired brain cholesterol dynamics and/or associated neurotransmission and synaptic plasticity failure. Part of this article was published as netprint and is available under the URL http://clinmed.netprints.org/cgi/content/full/2001100005v1. |
| Cholesterol, transferrin saturation, and the development of dementia and Alzheimer's disease: results from an 18-year population-based cohort Mainous, A. G., 3rd, S. L. Eschenbach, et al. (2005), Fam Med 37(1): 36-42. Abstract: BACKGROUND AND OBJECTIVES: Oxidative stress plays a role in Alzheimer's disease (AD), and iron and cholesterol together have been linked to oxidative stress. This study examined the relationship between transferrin saturation (TS) and cholesterol to see if both are necessary to increase the risk for the subsequent development of AD. METHODS: We analyzed data from US adults (ages 40-74 years at baseline) followed from baseline in 1971-1974 to 1992 (n=6,558) in the cohort study, the National Health and Nutrition Examination Survey I Epidemiologic Followup Study (NHEFS). RESULTS: The unadjusted relative risk of developing AD when both TS and cholesterol were at the 75th percentile was 3.19 (95% CI, 1.31-7.75). In adjusted models when only one marker was elevated, there was no significant increased risk for AD. The risk of AD increased as both markers increased. Even at the 85th percentile, individuals had no significant risk of AD when only having elevated cholesterol (>280 mg/dl) but not elevated TS (39.6%). Findings were similar for individuals with elevated TS but not elevated cholesterol. CONCLUSIONS: In this population-based cohort, the risk of developing AD when one has both elevated cholesterol and elevated TS is much larger than the risk associated with elevation of either of these factors alone. |
| Cholesterol, triacylglicerols and phospholipids during Xenopus embryo development Rizzo, A. M., R. Gornati, et al. (1994), Cell Biol Int 18(11): 1085-90. Abstract: Cholesterol, triacylglicerol and phospholipid content was analysed in Xenopus embryos during their early development (from day 1 to day 6). Triacylglicerols decrease significantly during the analysed stages and this can be explained by their use as energy substrate. Cholesterol and phospholipids, on the contrary, remain constant and are probably redistributed inside the embryo. The different phospholipid classes were separated by HPTLC. A constant decrease of PC and a marked increase of PS has been observed. The fatty acid composition of the single phospholipid classes has been analysed. |
| Cholesterol, triglycerides and lipoproteins in the serum of healthy, normal weight children between 6 and 12 years of age Zwiauer, K., H. Steininger, et al. (1990), Wien Klin Wochenschr 102(10): 299-303. Abstract: Serum cholesterol, triglycerides and lipoproteins were investigated in 276 healthy, prepubertal children and adolescents of normal weight aged 6 to 12 years. The results were evaluated on the basis of the guidelines of the Austrian Cholesterol Consensus Conference 1988 and according to the 90th and 95th percentiles of the Lipid Research Clinics (LRC) data. A relatively high percentage of the probands revealed cholesterol concentrations which could be classified as "risk" (50% of the female and 53% male probands) or "high risk" (39% of the girls and 25% of the boys). Classifying the cholesterol data according to the LRC criteria 46% of the girls and 41% of the boys exceeded these "cut off" values of the 90th percentile. Our data show that the mean serum cholesterol concentrations in healthy children and adolescents of normal weight--like in other European countries--are in a region concomitant with the category in adults which is associated with an increased risk for cardiovascular diseases. We assume that apart from genetic factors a high fat intake might play a predominant role in causing these raised levels. |
| Cholesterol, violent death, and mental disorder Ryman, A. (1994), Bmj 309(6952): 421-2. |
| Cholesterol. A review of the new directives Becker, D. M., J. H. Larosa, et al. (1990), Servir 38(6): 283-6. |
| Cholesterol. How low should we go? Chamsi-Pasha, H. (2005), Saudi Med J 26(1): 11-8. Abstract: The National Cholesterol Education Program NCEP has recently updated their Adult Treatment Panel (ATP) III guidelines and called for more intensive cholesterol treatment, especially in patients at high risk for coronary heart disease CHD. The message from the updated report is that lower is better for high risk patients, with the NCEP expert panel calling for low-density lipoprotein LDL- cholesterol treatment targets of <100 mg/dL in patients at high risk for CHD. In very high risk patients, however, aggressively lowering LDL-cholesterol to <70 mg/dL is now a therapeutic option for clinicians. Very high risk individuals are those with cardiovascular disease plus diabetes, persistent cigarette smoking, poorly controlled hypertension, or multiple risk factors of the metabolic syndrome, and those who recently had a myocardial infarction MI. Despite the strong clinical evidence and widely publicized treatment guidelines, many hyperlipidemic patients receive inadequate lipid-lowering treatment or leave the hospital after having a MI without a statin. Intensive therapy should be considered for all patients admitted to the hospital for acute coronary syndrome. Achieving very low levels of LDL-cholesterol often requires high doses of a statin or a combination therapy. The coadministration of ezetimibe, a new cholesterol-absorption inhibitor, further reduced LDL-cholesterol by 23% compared with those patients who remained on statin therapy alone. Recent trials with statin therapy are discussed in this review. |