| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| HDL receptor SR-BI and cholesterol gallstones Rigotti, A., S. Zanlungo, et al. (2002), Hepatology 35(1): 240-2. |
| HDL receptor-mediated cholesterol efflux from cells and its regulation Bierman, E. L., J. Oram, et al. (1991), Adv Exp Med Biol 285: 81-3. |
| HDL receptors and cholesterol efflux from parenchymal cells Slotte, J. P. (1990), Eur Heart J 11 Suppl E: 212-7. Abstract: High-density lipoproteins are thought to play an important role in the initial steps of reverse cholesterol transport in which cholesterol is removed from peripheral tissues to the liver for ultimate excretion. Since the cell types involved have been shown to possess high-affinity binding sites for HDL, it has been of considerable interest to find out whether or not these bindings sites are also involved in efflux of cholesterol from cells. Studies conducted in several laboratories have consistently shown that the binding site does not promote or enhance efflux of cholesterol from cellular plasma membrane. Binding of HDL to its cell surface binding site does, however, appear to promote efflux of cholesterol from intracellular compartments. The activity of the HDL binding sites has also been shown to be metabolically regulated in response to changes in the growth state and cholesterol homeostasis of the cell. It is therefore apparent that the binding sites are involved in a physiologically regulated process of cholesterol removal from cells, as part of reverse cholesterol transport. |
| HDL3-mediated cholesterol efflux from cultured enterocytes: the role of apoproteins A-I and A-II Herold, G., U. Hesse, et al. (1994), Lipids 29(11): 735-45. Abstract: High density lipoproteins (HDL) were recently demonstrated in an enterocyte model (CaCo-2 cells) to mediate reverse cholesterol transport by retroendocytosis. The present study was carried out to define the role of the major HDL apoproteins (apo) A-I and apo A-II in this pathway. HDL3 was fractionated by heparin affinity chromatography into the two main fractions containing either apo A-I only (fraction A) or both apo A-I and apo A-II (fraction B). In addition, liposomes were reconstituted from purified apo A-I or apo A-II and dimyristoyl phosphatidylcholine. The cell binding properties and cholesterol efflux potential were studied in the lipoprotein fractions and the liposomes. Both fractions exhibited similar maximal binding capacities of 4427 (A) and 5041 (B) ng/mg cell protein, but their dissociation constants differed (40.5 and 167.7 micrograms/mL, respectively). Fraction A induced cholesterol efflux and stimulated cholesterol synthesis more than did fraction B. Fraction A mobilized both cellular free and esterified cholesterol, whereas fraction B preferentially mobilized cholesteryl esters. Liposomes, containing either apo A-I or apo A-II, showed specific binding, endocytosis and endosomal transport, and were released as intact particles. Apo A-I liposomes also mediated cholesterol efflux. In conclusion, there is evidence that the HDL3 subfractions A and B, as well as reconstituted liposomes containing either apo A-I or apo A-II, were specifically bound and entered a retroendocytosis pathway which was directly linked to cholesterol efflux. Quantitatively, the apo A-I subfraction appeared to play the dominant role in normal enterocytes. The apo A-II content of fraction B was related to the mobilization of cholesteryl esters. |
| HDL3-retroendocytosis in cultured small intestinal crypt cells: a novel mechanism of cholesterol efflux Rogler, G., G. Herold, et al. (1991), Biochim Biophys Acta 1095(1): 30-8. Abstract: The present study in IEC-6 crypt-derived rat epithelial cells describes a retroendocytotic pathway for HDL3. These intestinal cells exhibited specific binding of apoE free HDL3 with a maximal binding capacity of 2980 ng/mg cell protein and a Kd of 36.4 micrograms/ml. Specific binding was competed for by HDL3 but not by LDL. Apparent internalisation of HDL3 was low, degradation was negligible and intact particles were resecreted into the medium within 2 h. Electron microscopic studies showed binding and internalisation of gold-labeled HDL3 in coated pit regions and transport in endosomes distinct from lysosomes to lipid droplets. De novo cholesterol synthesis from 14Coctanoate was enhanced nearly 2-fold by HDL3 and the surplus of newly formed cholesterol was recovered in the medium. It was concluded that intact HDL3 was bound specifically to intestinal cells and was resecreted through a process of retroendocytosis probably mediating efflux of cellular cholesterol. |
| HDL-binding protein on reverse cholesterol transport system Matsuyama, A. and S. Yamashita (2001), Nippon Rinsho 59 Suppl 2: 395-9. |
| HDL-cholesterol Nakai, T. and K. Oida (1995), Nippon Rinsho 53 Su Pt 1: 617-22. |
| HDL-cholesterol-- active or passive participant in the pathogenesis of atherosclerosis Artenie, R., D. Ungureanu, et al. (2003), Rev Med Chir Soc Med Nat Iasi 107(2): 282-7. Abstract: It is known that high sanguin levels of cholesterol and LDL-cholesterol (LDLc) have an important role in the pathogenesis of atherosclerosis. The treatment of hypercholesterolemia with statins and/or with fibrates have had beneficial effects on coronary heart disease and on other localization of atherosclerosis. The decreased of cholesterol and LDL-cholesterol is the most important effect of this treatment. The epidemiological studies have revealed that the treatment with statins and/or with fibrates produce an increase of HDL-cholesterol (HDLc), which is also very important in the regression of atherosclerosis. We tried in this review to explain the mechanisms of the increase of HDL-cholesterol, in concordance with the data from literature. |
| HDL-cholesterol and breast cancer: a joint study in northern Italy and southern France Ferraroni, M., M. Gerber, et al. (1993), Int J Epidemiol 22(5): 772-80. Abstract: The goal of the present study is to evaluate HDL-cholesterol (HDL-C) as a marker of breast cancer (BC) risk. It is based on several epidemiological and biological studies and is justified by the rising incidence of breast cancer throughout the world. A hospital-based study on host-related risk factors and breast cancer, conducted with similar methods in northern Italy and southern France, provided the biological data, the information on the established BC risk factors and on nutrition for 307 cases and 329 controls. This data set allowed for a thorough analysis of the relationship of HDL-C with established risk factors for BC and also of its association with BC at the time of diagnosis. Most of our findings on HDL-C determinants in the control sample are comparable to previous studies. The BC risk factors associated with reproductive life correlate with HDL-C levels: the protective factors are associated with a lower level of HDL-C and inversely. The same is true for nutritional factors such as alcohol. For these determinants, the trend is similar for cases and controls, and HDL-C level appears to be related to oestrogen metabolism. Thus it may be considered as a marker of BC risk. Our results indicate that high HDL-C levels should be especially checked in women aged > or = 60 years, or in premenopausal women presenting a low BMI, or in postmenopausal women with an early menopause. |
| HDL-cholesterol and cardiac disease: which table to use? Bayly, G. (2002), Ann Clin Biochem 39(Pt 1): 12-21. Abstract: Interventions to modify cardiovascular risk factors have the greatest benefit in individuals at greatest risk of a cardiovascular event, not necessarily those with the most extreme levels of any particular risk factor. Patients with vascular disease are readily identified, but risk calculation in those without disease provides a way of integrating several risk factors to identify individuals at greatest risk. Equations have been derived from different epidemiological studies (Framingham, PROCAM, etc.) to estimate the risk of different clinical end-points coronary heart disease (CHD) or cardiovascular disease (CVD). Some algorithms have been adapted to produce risk charts' or 'tables'; others have been modified to incorporate additional risk factors. Current UK guidelines all endorse calculation of CHD risk using the Framingham algorithm. This predicts risk well for some North European populations but less reliably in low-risk populations. It does not incorporate some risk factors, including serum triglycerides, family history, C-reactive protein, or homocysteine. Risk calculation should not be used in those with evidence of vascular disease, genetic hyperlipidaemia or a strong family history of CHD, and should be interpreted with caution in non-Caucasians. Measurement of high-density lipoprotein (HDL)-cholesterol is essential for accurate risk calculation. This has significant cost and workload implications for the laboratory. The way a laboratory reports results should be designed in such a way as to facilitate simple and accurate risk calculation. |
| HDL-cholesterol and the treatment of coronary heart disease: contrasting effects of atorvastatin and simvastatin Mikhailidis, D. P. and A. S. Wierzbicki (2000), Curr Med Res Opin 16(2): 139-46. Abstract: Although the levels of low-density lipoprotein (LDL) cholesterol remain the main therapeutic goal when treating dyslipidaemias, there is a need to consider high-density lipoprotein (HDL) concentrations. This conclusion is based on the findings of epidemiological surveys and appropriately designed trials using statins or fibrates. The importance of HDL, as a 'protective' lipoprotein fraction, has been recognised by major treatment guidelines. This review considers the differences in HDL-raising capacity of two of the most commonly prescribed statins--atorvastatin and simvastatin. When compared with simvastatin, atorvastatin is associated with progressively decreasing rises in the levels of HDL as the dose increases (negative dose response), an effect not reported with other statins. In contrast, simvastatin shows a positive dose response (increasing concentrations of HDL with increasing dose). This effect is paralleled by changes in apolipoprotein A-I levels. Apolipoprotein A-I is the main apolipoprotein associated with HDL. This dissimilarity in HDL response is an example of several differences that have been reported when comparing various statins. If 'all statins are not created equal', we should focus prescribing on those statins that have end point evidence originating from appropriately designed trials. |
| HDL-cholesterol as a marker of coronary heart disease risk: the Quebec cardiovascular study Despres, J. P., I. Lemieux, et al. (2000), Atherosclerosis 153(2): 263-72. Abstract: BACKGROUND: Primary as well as secondary prevention trials have shown the relevance of lowering LDL-cholesterol to reduce coronary heart disease (CHD) risk. However, although the association between LDL-cholesterol and CHD is well recognized, there is a considerable overlap in the distribution of plasma LDL-cholesterol levels between CHD patients and healthy subjects. The objective of the present review article is to use data from the Quebec cardiovascular study to demonstrate that in men, a low HDL-cholesterol may be even more of a risk factor and a target for therapy than a high LDL-cholesterol. METHODS AND RESULTS: Results of the Quebec cardiovascular study, a prospective study of 2103 middle-aged men followed for a period of 5 years, have confirmed results of previous studies in showing that plasma HDL-cholesterol concentration was an independent predictor of a first ischemic heart disease (IHD) event which included typical effort angina, coronary insufficiency, nonfatal myocardial infarction and coronary death. In addition, a reduced plasma HDL-cholesterol concentration was found to have a greater impact than raised LDL-cholesterol on the atherogenic index (total cholesterol/HDL-cholesterol ratio), this ratio being the best variable of the traditional lipid profile for the prediction of IHD events in the Quebec cardiovascular study. However, a low HDL-cholesterol concentration is not often observed as an isolated disorder but also includes hypertriglyceridemia, elevated apo B concentration, and an increased proportion of small, dense LDL particles. These abnormalities are features of an insulin resistant-hyperinsulinemic state resulting from abdominal obesity. CONCLUSIONS: It is therefore recommended that we need to go beyond LDL-cholesterol measurement lowering therapy for the optimal management of CHD risk. Raising plasma HDL-cholesterol through weight loss and a healthy diet, by an increased physical activity and, if required, by proper pharmacotherapy is therefore a legitimate therapeutic target for the optimal prevention of CHD in a large proportion of high risk patients. |
| HDL-cholesterol as a risk factor in coronary heart disease. An update of the Helsinki Heart Study Frick, M. H., V. Manninen, et al. (1990), Drugs 40 Suppl 1: 7-12. Abstract: The aim of the Helsinki Heart Study, a 5-year primary prevention placebo-controlled study involving 4081 dyslipidaemic men (aged 40 to 55 years), was to investigate if increasing high density lipoprotein (HDL)-cholesterol plasma levels and decreasing low density lipoprotein (LDL)-cholesterol levels would reduce the incidence of coronary heart disease. Gemfibrozil 600mg twice daily was administered to induce these changes in lipoprotein levels. Baseline HDL-cholesterol levels in the study group were similar to those in the general population. Data from patients treated with placebo were analysed to investigate the influence of HDL-cholesterol levels on the incidence of coronary heart disease. Using the number of cardiac end-points per 1000 person-years to indicate the risk of coronary heart disease, it was clear that elevated HDL-cholesterol levels reduced the risk of coronary heart disease while the incidence increased at low HDL-cholesterol levels. This relationship was not altered when the effect of HDL-cholesterol levels was analysed jointly with other coronary risk factors (age, smoking or blood pressure). A weaker association was seen between LDL-cholesterol and risk of coronary heart disease, and triglycerides appeared to have no significant effect on the incidence of the disease. The data clearly suggest that HDL-cholesterol is a strong predictor of the incidence of coronary heart disease in the placebo group of the Helsinki Heart Study. |
| HDL-cholesterol increase associated to triglycerides degradation in vitro Jimeno, B., M. A. Zubeldia, et al. (1995), Rev Esp Fisiol 51(2): 101-4. Abstract: The effect of muscle tissue from rats trained by swimming on the extracellular degradation of triglyceride (TG) rich particles has been studied in vitro. During incubation, there is a progressive decline of the TG concentration in the incubation medium. At the end of the incubation period (90 min), a significantly reduction in the TG levels (p < 0.05) is associated with a significant increase in the high-density lipoprotein (HDL) cholesterol level (p < 0.005). There are no significant changes in total cholesterol levels. The correlation of the TG decline with the HDL-cholesterol increase is significant (r = 0.695, p < 0.05, n = 25). The experimental model used here could be of great interest for the in vitro study of factors affecting lipid levels in plasma. |
| HDL-cholesterol level and cortisol response to synacthen in critically ill patients van der Voort, P. H., R. T. Gerritsen, et al. (2003), Intensive Care Med 29(12): 2199-203. Abstract: OBJECTIVE: To explore the relationship between cholesterol levels and the adrenal cortisol response to synacthen in critically ill patients. DESIGN: Prospective observational study. PATIENTS: Critically ill patients with multiple organ dysfunction syndrome (MODS) with possible adrenal dysfunction defined as unexplained hypotension, ongoing inotropic support, unexplained fever, unexplained hyponatraemia or a combination of these symptoms. MEASUREMENTS: HDL-cholesterol levels (HDL), total cholesterol levels (TC), and triglycerides (TG) before administration of synacthen. LDL-cholesterol was calculated using the Friedewald formula. Basal cortisol and response to 250 microg synacthen intravenously was measured. A cortisol rise of 0.25 micromol/l in a 30-min or 60-min blood sample after synacthen infusion was defined as a proper adrenal response. RESULTS: Patients with a proper response to synacthen showed higher HDL-cholesterol levels than patients without that response (P=0.02). Severity of disease as measured by APACHE II or SOFA was not a confounder. LDL-cholesterol levels were extremely low in both responders and non-responders and were not associated with the absolute rise in cortisol. In linear and logistic regression analysis HDL-cholesterol was the sole predictor of cortisol response. CONCLUSIONS: Adrenal cortisol response to a "classic" 250-microg synacthen test relates in critically ill patients to HDL-cholesterol levels. LDL and TC levels did not show such a relation. These findings are in concordance with known biochemical pathways of cortisol production. |
| HDL-cholesterol or apolipoprotein AI: which parameter to choose? Bigot-Corbel, E., M. C. Amory-Touz, et al. (1996), Ann Biol Clin (Paris) 54(10-11): 349-52. Abstract: The French Consensus for cholesterol, established by ARCOL in 1989, recommends the use of HDL-cholesterol and apolipoprotein AI as additional parameters. The present study was undertaken to establish the correlation between these two parameters and to determine the limit value for apolipoprotein AI, based on the recommended limit of 0.90 mmol/L for HDL-cholesterol established by ARCOL. The correlation between HDL-cholesterol analysed by precipitation, and apolipoprotein AI analysed by immunonephelemetry on the day of blood drawing, determined on 1980 samples, raised a r value of 0.89. Using the regression line equation (y = 0.602 x + 0.629), the apolipoprotein AI value corresponding to the recommended HDL-cholesterol limit (0.90 mmol/L) was found to be 1.17 g/L, while the limit value established by ARCOL was 1.20 g/L. Using the HDL-cholesterol value of 0.90 mmol/L, the population was divided into a high risk group and a low risk group. With the limit value of 1.20 g/L for apolipoprotein AI, 89.2% of the subjects would be correctly classified. This percentage would be raised to 90.65% using the value (1.17 g/L) established in our study. Our conclusion is that apolipoprotein AI as well as HDL-cholesterol represent good markers for atherosclerosis in the clinical practice. The advantage of HDL-cholesterol is that the determination of this parameter allows the calculation of LDL-cholesterol which is used in all consensus, while the advantage of apolipoprotein AI is that it may be analysed automatically. |
| HDL-cholesterol reductions associated with adult growth hormone replacement Leese, G. P., M. Wallymahmed, et al. (1998), Clin Endocrinol (Oxf) 49(5): 673-7. Abstract: OBJECTIVE: To study the effects of human growth hormone (hGH) replacement on serum lipids and lipoprotein (a) (Lp(a)) concentrations. DESIGN: A randomized double blind placebo controlled trial for 6 months followed by an open trial where all patients were treated with hGH for a further 6 months. Treatment was with recombinant hGH given in a dose of 0.125U/kg/wk increasing to 0.25U/Kg/wk. PATIENTS: Thirty two patients with growth hormone deficiency were recruited, but two withdrew because of side effects. Of the thirty patients (age 35.1 +/- 11.8 year; mean +/- SD) completing the study 13 of were assigned to the placebo group for six months and 17 to active treatment from the start. MEASUREMENTS: Fasting serum samples were analysed for total cholesterol, High density lipoprotein (HDL)-cholesterol, HDL-subfractions, triglycerides, lipoprotein (a) (Lp(a)) and IGF-1. LDL-cholesterol was calculated using the Friedewald formula. RESULTS: Compared to placebo, 6 months treatment with hGH therapy resulted in increased IGF-1 (37.6 +/- 4.1 vs. 14.0 +/- 2.2 nmol/l, P < 0.01), but there was no significant difference in any of the lipid parameters measured between placebo and active treatment groups at 6 months. hGH was associated with a decrease in HDL-cholesterol concentration from baseline to 6 months (0.97 +/- 0.08 to 0.76 +/- 0.10 mmol/l P < 0.01), especially within the HDL2 subfraction. This reduction was maintained at 12 months. There was no change in Lp(a) concentrations from 0 to 6 months (placebo -26 (-340 to 82), median and range, active -4 (-586 to 212) mg/l). There was no change in total cholesterol, LDL-cholesterol, triglycerides or proportion of HDL subfractions. CONCLUSIONS: Treatment with hGH can reduce serum HDL-cholesterol concentrations. Further investigation of this is required. |
| HDL-cholesterol testing Tallis, G. A., D. W. Thomas, et al. (1990), Med J Aust 153(6): 364-5. |
| HDL-Cholesterol, total cholesterol, and the risk of stroke in middle-aged British men Wannamethee, S. G., A. G. Shaper, et al. (2000), Stroke 31(8): 1882-8. Abstract: BACKGROUND AND PURPOSE: The purpose of this study was to examine the relation between serum HDL cholesterol and total cholesterol and risk of stroke. METHODS: We carried out a prospective study in 7735 men, 40 to 59 years of age, drawn from 1 group practice in each of 24 British towns. Men with history of stroke were excluded (n=52). RESULTS: During the mean follow-up period of 16.8 years, there were 343 stroke cases (fatal and nonfatal) in the 7683 men with no history of stroke. Higher levels of HDL cholesterol were associated with a significant decrease in risk of stroke even after adjustment for potential confounders (top fifth versus lowest fifth: adjusted relative risk=0.68, 95% CI 0.46 to 0.99). The inverse relation was seen only for nonfatal strokes (adjusted relative risk=0.59, 95% CI 0.39 to 0.90; top fifth versus lowest fifth). Total cholesterol showed no graded association with fatal strokes, but men with levels > or =8.1 mmol/L (top 5% of the distribution) showed increased risk of nonfatal stroke, although this was not statistically significant after adjustment (adjusted RR=1.46, 95% CI 0.91 to 2.32). The beneficial effects of elevated HDL cholesterol on nonfatal stroke were seen in both smokers and nonsmokers and were more evident in men with hypertension than in normotensives. In hypertensive men, elevated HDL cholesterol (top fifth) was associated with a significant 50% reduction in risk of nonfatal strokes compared with men in the lowest fifth. CONCLUSIONS: Higher levels of HDL cholesterol were associated with a significant decrease in risk of nonfatal stroke. In contrast, elevated total cholesterol showed a weak positive association with nonfatal strokes. The marked inverse association between HDL cholesterol and stroke seen in hypertensives emphasizes the importance of those modifiable risk factors for stroke known to lower the concentrations of HDL cholesterol. |
| HDL-cholesterol: exercise formula. Results of long-term (6-year) strenuous swimming exercise in a middle-aged male with paraplegia Sorg, R. J. (1993), J Orthop Sports Phys Ther 17(4): 195-9. Abstract: Paraplegic individuals are at increased risk for developing heart disease because of low HDL-cholesterol levels. Exercise has been identified as an important factor in raising the HDL-cholesterol level. This case study documents the effects of long-term (6-year) strenuous exercise (2940 kcal/wk) on lipid markers in a 41-year-old white male with paraplegia. An additional 21 mg of HDL-cholesterol (84% increase) were observed in a paraplegic individual who swam 2100 kcal/week for 6 years. Througout this study, serial blood samples were analyzed for total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglycerides. An initial low HDL-cholesterol of 25 mg/dl was measured in the subject. This case study continued for 72 months to determine the long-term effects on various blood lipid fractions of swimming an additional 2.5 hours/week. HDL-cholesterol slowly increased over the duration of the study. After 12 months of swimming the HDL fraction had increased from 25 mg/dl to 31 mg/dl. After 24 months and at the end of 72 months of swimming, the HDL fraction had risen to 43 mg/dl and 46 mg/dl, respectively. The estimated long-term energy cost for each additional 1 mg/dl of HDL-cholesterol above the pre-exercise HDL value was 100 kcal/week in this subject. Long-term strenuous swimming exercise has been successfully incorporated into the lifestyle of a paraplegic individual. Significant reduction in known coronary risk factors followed a marked increase in the HDL-cholesterol level. |