| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| High-density lipoproteins from probucol-treated patients have increased capacity to promote cholesterol efflux from mouse peritoneal macrophages loaded with acetylated low-density lipoproteins Ishigami, M., S. Yamashita, et al. (1997), Eur J Clin Invest 27(4): 285-92. Abstract: To elucidate the anti-atherogenic effect of probucol, high-density lipoprotein (HDL) was isolated from probucol-treated patients (n = 14) and compared with that from control subjects (n = 12). The HDL obtained from probucol-treated patients was low in cholesteryl ester (CE) in comparison with that from control subjects (21.3 +/- 3.9 mol per cent vs. 27.6 +/- 3.2 mol% of total lipids. P < 0.001), and the peak diameters of patients' HDL were significantly smaller than those of control subjects on 4-30% non-denaturing polyacrylamide gradient gel electrophoresis (10.6 +/- 0.6 nm vs. 12.1 +/- 0.4 nm, P < 0.001). These data may be explained by the increased cholesteryl ester transfer protein (CETP) activities of probucol-treated patients (129 +/- 12% of control subjects, P < 0.001). The in vitro ability of HDL to remove CE from lipid-laden macrophages induced by incubation with acetylated low-density lipoprotein (Ac-LDL) was studied. The small and CE-poor HDL obtained from probucol-treated patients had a greater capacity to promote CE efflux from macrophages than did control HDL (59.8 +/- 6.9% vs. 44.2 +/- 5.4%, P < 0.01). Furthermore, the ability of HDL to promote cholesterol efflux correlated negatively with the CE content and particle diameter of HDL (r = -0.561 and r = -0.583 respectively; P < 0.01). When the inhibitory effect of HDL on the incorporation of 14C-oleate into cellular cholesteryl ester was compared, the HDL from patients and control subjects inhibited CE formation to a similar extent. The enhanced ability of probucol-treated patients' HDL may, therefore, be involved in the acceleration of hydrolysis of the CE pool in macrophages. Taken together, we conclude that CETP plays a crucial role in making HDL more active in its anti-atherogenic function by reducing CE and making HDL smaller, and that probucol may enhance reverse cholesterol transport by activating CE transfer in vivo. The current study demonstrated, for the first time, that HDL modified by enhanced CETP activity in vivo is potentially anti-atherogenic. |
| High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age Weverling-Rijnsburger, A. W., I. J. Jonkers, et al. (2003), Arch Intern Med 163(13): 1549-54. Abstract: BACKGROUND: A high total serum cholesterol level does not carry a risk of cardiovascular mortality among people 85 years and older and is related to decreased all-cause mortality. At this old age, there are few data on fractionated lipoprotein levels in the determination of cardiovascular disease risk. The aim of this study was to evaluate the relationships between low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels and mortality from specific causes among people in the oldest age categories. METHODS: Between September 1, 1997, and September 1, 1999, a total of 705 inhabitants in the community of Leiden, the Netherlands, reached the age of 85 years. Among these old people, we initiated a prospective follow-up study to investigate determinants of successful aging. A total of 599 subjects participated (response rate, 87%) and all were followed up to September 2001. Serum levels of total, LDL, and HDL cholesterol were assessed at baseline along with detailed information on comorbid conditions. The main outcome measure was all-cause and specific mortality risk. RESULTS: During 4 years of follow-up, 152 subjects died. The leading cause of death was cardiovascular disease, with similar mortality risks in all tertiles of LDL cholesterol level. In contrast, low HDL cholesterol level was associated with a 2.0-fold higher risk of fatal cardiovascular disease (95% confidence interval CI, 1.2-3.2). The mortality risk of coronary artery disease was 2.0 (95% CI, 1.0-3.9) and for stroke it was 2.6 (95% CI, 1.0-6.6). Both low LDL cholesterol and low HDL cholesterol concentrations were associated with an increased mortality risk of infection: 2.7 (95% CI, 1.2-6.2) and 2.4 (95% CI, 1.1-5.6), respectively. The risks were unaffected by comorbidity. CONCLUSION: In contrast to high LDL cholesterol level, low HDL cholesterol level is a risk factor for mortality from coronary artery disease and stroke in old age. |
| High-density-lipoprotein cholesterol and atherosclerosis Ng, D. S. and R. A. Hegele (1993), Cmaj 149(12): 1807-8. |
| High-density-lipoprotein cholesterol and types of alcoholic beverages consumed among men and women Parker, D. R., J. B. McPhillips, et al. (1996), Am J Public Health 86(7): 1022-7. Abstract: OBJECTIVES. Differences by sex in the relationship between high-density-lipoprotein (HDL) cholesterol and consumption of alcoholic beverages were examined in 1516 individuals. METHODS. Questionnaires and blood-sample data from cross-sectional surveys were analyzed. RESULTS. Both beer and liquor were independently associated with increased HDL cholesterol in the total group, in men, and in women after covariates were controlled for. Wine was associated with a significant increase in HDL cholesterol in women only. CONCLUSIONS. Among women and men, amount may be more important than type of alcoholic beverage consumed. The independent effect of wine on HDL cholesterol among men remains unclear since few men in this population consumed wine exclusively or in large quantities. |
| High-density-lipoprotein-induced cholesterol efflux from arterial smooth muscle cell derived foam cells: functional relationship of the cholesteryl ester cycle and eicosanoid biosynthesis Pomerantz, K. B. and D. P. Hajjar (1990), Biochemistry 29(7): 1892-9. Abstract: Eicosanoids have been implicated in the regulation of arterial smooth muscle cell (SMC) cholesteryl ester (CE) metabolism. These eicosanoids, which include prostacyclin (PGI2), stimulate CE hydrolytic activities. High-density lipoproteins (HDL), which promote cholesterol efflux, also stimulate PGI2 production, suggesting that HDL-induced cholesterol efflux is modulated by eicosanoid biosynthesis. To ascertain the role of endogenously synthesized eicosanoids produced by arterial smooth muscle cells in the regulation of CE metabolism, we examined the effects of cyclooxygenase inhibition on CE hydrolytic enzyme activities, cholesterol efflux, and cholesterol content in normal SMC and SMC-derived foam cells following exposure to HDL and another cholesterol acceptor protein, serum albumin. Alterations of these activities were correlated with cholesterol efflux in response to HDL or bovine serum albumin (BSA) in the presence or absence of aspirin. HDL stimulated PGI2 synthesis and CE hydrolases in a dose-dependent manner. Eicosanoid dependency was established by demonstrating that HDL-induced acid cholesteryl ester hydrolase (ACEH) activity was blocked by aspirin. CE enrichment essentially abrogated HDL-induced PGI2 production in cells which also exhibited decreased lysosomal and cytoplasmic CE hydrolase activities. In CE-enriched cells whose cytoplasmic CE pool was metabolically labeled with 3Holeate or cLDL containing 3Hcholesteryl linoleate, aspirin did not alter HDL- or BSA-induced net CE hydrolysis or efflux, respectively. Finally, aspirin treatment did not alter the mass of either free or esterified cholesterol content of untreated or CE-enriched SMC following exposure to acceptor proteins. These data demonstrated that CE enrichment significantly reduced HDL-induced activation of CE hydrolytic activity via inhibition of endogenous PGI2 production.(ABSTRACT TRUNCATED AT 250 WORDS) |
| High-dose recombinant apolipoprotein A-I(milano) mobilizes tissue cholesterol and rapidly reduces plaque lipid and macrophage content in apolipoprotein e-deficient mice. Potential implications for acute plaque stabilization Shah, P. K., J. Yano, et al. (2001), Circulation 103(25): 3047-50. Abstract: BACKGROUND: Repeated doses of recombinant apolipoprotein A-I(Milano) phospholipid complex (apoA-I(m)) reduce atherosclerosis and favorably change plaque composition in rabbits and mice. In this study, we tested whether a single high dose of recombinant apoA-I(m) could rapidly mobilize tissue cholesterol and reduce plaque lipid and macrophage content in apoE-deficient mice. METHODS AND RESULTS: High cholesterol-fed, 26-week-old apoE-deficient mice received a single intravenous injection of saline (n=16), 1080 mg/kg dipalmitoylphosphatidylcholine (DPPC; n=14), or 400 mg/kg of recombinant apoA-I(m) complexed with DPPC (1:2.7 weight ratio; n=18). Blood was sampled before and 1 and 48 hours after injection, and aortic root plaques were evaluated for lipid content and macrophage content after oil-red O and immunostaining, respectively. One hour after injection, the plasma cholesterol efflux-promoting capacity was nearly 2-fold higher in recombinant apoA-I(m)-treated mice compared with saline and DPPC-treated mice (P<0.01). Compared with baseline values, serum free cholesterol, an index of tissue cholesterol mobilization, increased 1.6-fold by 1 hour after recombinant apoA-I(m) injection, and it remained significantly elevated at 48 hours (P<0.01). Mice receiving recombinant apoA-I(m) had 40% to 50% lower lipid content (P<0.01) and 29% to 36% lower macrophage content (P<0.05) in their plaques compared with the saline- and DPPC-treated mice, respectively. CONCLUSIONS: A single high dose of recombinant apoA-I(m) rapidly mobilizes tissue cholesterol and reduces plaque lipid and macrophage content in apoE-deficient mice. These findings suggest that this strategy could rapidly change plaque composition toward a more stable phenotype. |
| Higher cholesterol and insulin levels in pregnancy are associated with increased risk for pregnancy-induced hypertension Solomon, C. G., J. S. Carroll, et al. (1999), Am J Hypertens 12(3): 276-82. Abstract: Hyperinsulinemia and dyslipidemia are known to be associated with essential hypertension but their role in pregnancy-induced hypertension remains unclear. We performed a case-control study comparing cholesterol, insulin, and glucose levels in the early third trimester of pregnancy among 31 women who developed pregnancy-induced hypertension (PIH) (either preeclampsia n = 6 or nonproteinuric gestational hypertension n = 25), with 31 women remaining normotensive through pregnancy. As compared with women remaining normotensive, women subsequently developing PIH had higher fasting cholesterol levels (279 v 247 mg/dL; P =.02) and higher fasting insulin levels (13.3 v 7.9 microU/mL; P =.03), although fasting glucose levels and levels of glucose and insulin after glucose load did not differ significantly between groups. In comparing hypertensive subgroups, fasting insulin levels were significantly higher among women who subsequently developed preeclampsia, but not among those subsequently developing nonproteinuric gestational hypertension. Although women developing PIH had higher pregravid body mass index (25.1 v 22.6 kg/m2, P =.06), fasting cholesterol and insulin levels were associated with risk for PIH even after adjustment for body mass index and age (relative risks for one unit increase, respectively: 1.02 (P =.03) and 1.12 (P =.03). Higher fasting cholesterol and insulin levels in mid- to late pregnancy are associated with increased risk for PIH. These observations support a role for insulin resistance in the development of this complication of pregnancy. |
| Higher cholesterol in human LDL is associated with the increase of oxidation susceptibility and the decrease of antioxidant defence: experimental and simulation data Mosinger, B. J. (1999), Biochim Biophys Acta 1453(1): 180-4. Abstract: Increased low-density lipoprotein (LDL) cholesterol is a recognized risk factor for atherosclerosis. There is also strong evidence that oxidatively modified LDL initiates the development of this pathological process and the administration of antioxidants might have a protective effect. However, the appropriate trials did not provide completely consistent results. We found in this study that the oxidation kinetics and also the antioxidant effectiveness are different depending on the cholesterol content in LDL. Higher cholesterol in LDL causes an acceleration of its oxidation as well as an increase of resistance to the antioxidative effect of ascorbic acid. In searching for a theoretical background of this dual impact of cholesterol in LDL, computer simulation of LDL oxidation was used. It was found that the pre-existing level of lipid hydroperoxides together with the total amount of oxidizable lipid substrate associated with the cholesterol level in LDL were satisfactory prerequisites for a best fit to the experimental data. In conclusion, this study provides at least a partial explanation for some failures to arrest, by administration of antioxidants, the progression of atherosclerosis in animal and human hypercholesterolemia. |
| Higher high density lipoprotein cholesterol associated with moderate alcohol consumption is not related to altered plasma lecithin:cholesterol acyltransferase and lipid transfer protein activity levels Riemens, S. C., A. van Tol, et al. (1997), Clin Chim Acta 258(1): 105-15. Abstract: Lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) are important factors involved in HDL metabolism. Altered plasma activity levels of these factors could play a role in the increase in high density lipoprotein (HDL) cholesterol associated with moderate alcohol consumption. We measured plasma LCAT, CETP and PLTP activities with exogenous substrate assays, as well as lipoproteins and HDL lipids in 6 alcohol-abstaining men, 18 matched men who used < or = 1 and 18 men who used > or = 1 alcohol-containing drinks per day. Plasma cholesterol and triglycerides were similar in the three groups. HDL total cholesterol, HDL cholesteryl ester, HDL free cholesterol and HDL triglycerides were higher in the alcohol drinkers compared to the abstainers (all P < 0.05). No differences in plasma LCAT, CETP and PLTP activity levels were observed between the three groups. Analysis of covariance also demonstrated that the use of alcohol was associated with higher HDL cholesterol (P < 0.04), whereas plasma LCAT, CETP and PLTP activity levels were not related to alcohol consumption. Furthermore, HDL cholesteryl ester was positively associated with LCAT activity (P < 0.001), PLTP activity (P < 0.01) and alcohol intake (P < 0.04) and negatively with plasma triglycerides (P < 0.001) and CETP activity (P < 0.03); indicating that alcohol influenced HDL cholesteryl ester independently from these biochemical parameters. The higher HDL cholesterol associated with moderate alcohol consumption is, therefore, unlikely to be caused by and effect on plasma LCAT, CETP or PLTP activity levels. |
| Higher levels of plasma cholesterol sulfate in patients with liver cirrhosis and hypercholesterolemia Tamasawa, N., A. Tamasawa, et al. (1993), Lipids 28(9): 833-6. Abstract: An analytical method for the determination of cholesterol sulfate (CS) in plasma using gas-liquid chromatography was developed. We measured plasma CS concentrations in patients with liver cirrhosis and hypercholesterolemia as examples of disorders that involve aberrations in cholesterol metabolism. Patients with liver cirrhosis had plasma CS concentrations that were significantly higher than those of control subjects (444.6 +/- 51.7 vs. 253.0 +/- 24.6 micrograms/dL, mean +/- SE). The levels of other lipids were lower in cirrhotics, although the differences were not significant. There was no correlation between the levels of CS and sulfated bile acids in cirrhotic patients. CS levels in plasma were also higher in subjects with hypercholesterolemia (413.7 +/- 44.5 micrograms/dL); however, the ratio of CS to total cholesterol (TC) clearly differed between cirrhotics and hypercholesterolemic subjects (1.44 +/- 0.11 x 10(-3) vs. 3.31 +/- 0.63 x 10(-3); P < 0.05). Both in subjects with hypercholesterolemia and in healthy controls, the CS/TC ratio was similar and CS accounted for roughly 0.14% of the TC concentration. |
| Higher prevalence of depressive symptoms in middle-aged men with low serum cholesterol levels Steegmans, P. H., A. W. Hoes, et al. (2000), Psychosom Med 62(2): 205-11. Abstract: OBJECTIVE: Investigators from several studies have reported a positive relationship between low cholesterol levels and death due to violent causes (eg, suicide and accidents), possibly mediated by depressive symptoms, aggression or hostility, or impulsivity. We set out to establish whether middle-aged men with chronically low cholesterol levels (< or =4.5 mmol/liter) have a higher risk of having depressive symptoms, according to scores on the Beck Depression Inventory, compared with a reference group of men with cholesterol levels between 6 and 7 mmol/liter. A similar comparison was also made for measures of anger, hostility, and impulsivity. METHODS: Cholesterol measurements were obtained as part of a population-based cholesterol screening study in 1990-1991. These levels were remeasured in 1993-1994. Only those whose cholesterol level remained in the same range were included in the study. Depressive symptoms were assessed by using the Beck Depression Inventory; anger, by questionnaires based on the Spielberger Anger Expression Scale and State-Trait Anger Scale; hostility, by the Buss-Durkee Hostility Inventory; and impulsivity, by the Eysenck and Eysenck Impulsivity Questionnaire. RESULTS: Men with chronically low cholesterol levels showed a consistently higher risk of having depressive symptoms (Beck Depression Inventory score > or =15 or > or =17) than the reference group, even after adjusting for age, energy intake, alcohol use, and presence of chronic diseases. No differences in anger, hostility, and impulsivity were observed between the two groups. CONCLUSIONS: Men with a lower cholesterol level (< or =4.5 mmol/liter) have a higher prevalence of depressive symptoms than those with a cholesterol level between 6 and 7 mmol/liter. These data may be important in the ongoing debate on the putative association between low cholesterol levels and violent death. |
| Higher triglycerides, lower high-density lipoprotein cholesterol, and higher systolic blood pressure in lipoprotein lipase-deficient heterozygotes. A preliminary report Sprecher, D. L., B. V. Harris, et al. (1996), Circulation 94(12): 3239-45. Abstract: BACKGROUND: Heterozygous lipoprotein lipase (LPL) deficiency has been associated with familial hypertriglyceridemia and familial combined hyperlipidemia. Studies of heterozygotes with LPL gene defects at amino acid residues 188 and 207 showed higher triglycerides (TG) and lower HDL cholesterol (HDL-C), with no elevation in LDL cholesterol (LDL-C). Other LPL defects may reveal alternate clinical phenotypes. METHODS AND RESULTS: We evaluated three families with defects at amino acid residues 64, 194, and 188. Thirty-eight heterozygotes (8 with defect 64, 14 with defect 194, and 16 with defect 188) and 95 family members without defects were studied. Plasma lipid, lipoprotein, and apolipoprotein (apo) values were measured, as well as blood pressure. Pooled carriers demonstrated higher systolic blood pressure (SBP) (127 versus 116 mm Hg, P <.0001) and TG (160 versus 125 mg/dL, P =.004) and lower HDL-C (44 versus 52 mg/dL, P =.001) than did noncarriers. A comparison of the 188 carriers and noncarriers revealed the most striking phenotypic characteristics, with lower HDL-C (36 versus 51 mg/dL, P <.0001) and HDL-C/(apo A-I + apo A-II) (0.21 versus 0.24, P =.002) and higher TG (206 versus 123 mg/dL, P =.0003), SBP (132 versus 116 mm Hg, P =.0004), and apo B/LDL-C (1.12 versus 0.93, P <.0001). CONCLUSIONS: These data confirm past observations that LPL deficient heterozygotes trend toward lower HDL-C and higher TG levels while potentially expressing higher SBP. These data also implicate the specific LPL gene defect as a contributing factor to the variable expression of HDL-C, TG, and SBP. |
| High-fat spreadable processed cheese for people with high blood cholesterol Abou-Zeid, N. A. (1993), J Dairy Res 60(2): 239-45. Abstract: Part of the raw cheese base used for manufacturing high-fat processed cheese spread was replaced by cows' (C) or buffalo (B) butter residue at levels of up to 20%. These residues were produced during the conversion of butter to butter oil by traditional moderate (T) or severe (M) heat treatments. The hypocholesterolaemic properties of butter residues incorporated into processed cheese were tested with rats (serum and liver cholesterol) and human beings (serum cholesterol). When rats were given the control cheese with no butter residue there were significant increases in both serum and liver cholesterol compared with rats given stock diet. However, when part of the raw cheese base was replaced by butter residue these rises were reduced by amounts proportional to the level of butter residue. The hypocholesterolaemic properties of the residues were in order CT > BT, CM > BM, and incorporations of 10% CT, 15% BT, 15% CM and 20% BM were found to nullify the hypercholesterolaemic effects of control cheese and restore cholesterol levels to their normal values. A small human trial gave similar results. Incorporation of butter residue slightly affected the chemical composition of the cheeses. Fat content and pH were little different; however, cheeses with butter residue tended to have higher total protein but lower soluble protein, tyrosine and tryptophan, and total volatile fatty acids. Rheological properties were not altered significantly. Incorporation of butter residue improved the organoleptic properties, particularly flavour intensity. Storage at 5 degrees C for 2 months did not alter the organoleptic properties and changes in chemical composition followed the normal pattern. |
| High-fat, high-cholesterol diet increases the incidence of gastritis in LDL receptor-negative mice Laurila, A., S. P. Cole, et al. (2001), Arterioscler Thromb Vasc Biol 21(6): 991-6. Abstract: Transgenic and knockout mice are widely used as models for atherogenesis studies. While developing a Helicobacter infection model in LDL receptor-negative (LDLR(-/-)) mice, we noticed that mice fed a high-fat, high-cholesterol diet often contracted gastritis independent of infection. To further investigate this finding, we studied 27 male and 18 female LDLR(-/-) mice fed high-fat, 1% or 1.25% cholesterol diets for 3 to 4 months. The extent of atherosclerosis was morphometrically analyzed in the whole aorta, and the degree of gastric inflammation was scored histologically in hematoxylin-eosin-stained stomach sections. The autoantibody titers to epitopes of oxidized LDL were also measured. Mice fed high-fat, high-cholesterol diets had a significantly higher incidence of gastritis than mice fed normal chow, 62% versus 5%, respectively (P<0.0001). This effect was specific for LDLR(-/-) mice, because no difference in gastritis was found in wild-type mice fed either diet. Animals with gastritis showed slightly more atherosclerosis than animals without gastritis: 16.3+/-6.4% versus 12.8+/-3.4% in males and 9.4+/-3.5% versus 6.5+/-3.3% in females. Cholesterol-fed mice also had significantly higher IgG autoantibody titers against modified LDL than normal chow-fed animals, but no difference was seen between the gastritis and nongastritis groups. We conclude that the standard high-fat, high-cholesterol diet commonly used in many murine models to induce atherosclerosis increased the incidence of gastritis significantly in LDLR(-/-) mice. |
| High-fat, high-cholesterol diet raises plasma HDL cholesterol: studies on the mechanism of this effect Wolf, G. (1996), Nutr Rev 54(1 Pt 1): 34-5. Abstract: Earlier work with human subjects showed that a low-fat, low-cholesterol diet lowered plasma high-density-lipoprotein-cholesterol (HDL-C) and the production rate of apolipoprotein A-I (apo A-I). More recent research with transgenic mice demonstrated that a high-fat, high-cholesterol diet raised plasma HDL-C and the production rate of apo A-I by a mechanism involving the regulation of translation of the apo A-I mRNA. The authors conclude that the rise induced in HDL-C by a high-fat, high-cholesterol diet is defensive and therefore, should not be interpreted as a desirable dietary change. |
| High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men Davy, B. M., K. P. Davy, et al. (2002), Am J Clin Nutr 76(2): 351-8. Abstract: BACKGROUND: No studies have examined whether increased consumption of oat cereal, rich in soluble fiber, favorably alters lipoprotein particle size and number. OBJECTIVE: We examined the effects of large servings of either oat or wheat cereal on plasma lipids, lipoprotein subclasses, lipoprotein particle diameters, and LDL particle number. DESIGN: Thirty-six overweight men aged 50-75 y were randomly assigned to consume daily for 12 wk either oat or wheat cereal providing 14 g dietary fiber/d. Before and after the intervention, plasma lipid and lipoprotein subclasses were measured with proton nuclear magnetic resonance spectroscopy, and whole-body insulin sensitivity was estimated with the frequently sampled intravenous-glucose-tolerance test. RESULTS: Time-by-treatment interactions (P < 0.05) for LDL cholesterol (oat: -2.5%; wheat: 8.0%), small LDL cholesterol (oat: -17.3%; wheat: 60.4%), LDL particle number (oat: -5.0%; wheat: 14.2%), and LDL:HDL cholesterol (oat: -6.3%; wheat: 14.2%) were observed. Time-by-treatment interactions were nearly significant for total cholesterol (oat: -2.5%; wheat: 6.3%; P = 0.08), triacylglycerol (oat: -6.6%; wheat: 22.0%; P = 0.07), and VLDL triacylglycerol (oat: -7.6%; wheat: 2.7%; P = 0.08). No significant time-by-treatment interactions were observed for HDL cholesterol, HDL-cholesterol subclasses, or LDL, HDL, and VLDL particle diameters. Insulin sensitivity did not change significantly with either intervention. CONCLUSIONS: The oat compared with the wheat cereal produced lower concentrations of small, dense LDL cholesterol and LDL particle number without producing adverse changes in blood triacylglycerol or HDL-cholesterol concentrations. These beneficial alterations may contribute to the cardioprotective effect of oat fiber. |
| High-flux mitochondrial cholesterol trafficking, a specialized function of the adrenal cortex Jefcoate, C. (2002), J Clin Invest 110(7): 881-90. |
| High-frequency, spin-label EPR of nonaxial lipid ordering and motion in cholesterol-containing membranes Gaffney, B. J. and D. Marsh (1998), Proc Natl Acad Sci U S A 95(22): 12940-3. Abstract: The EPR spectra of spin-labeled lipid chains in fully hydrated bilayer membranes of dimyristoyl phosphatidylcholine containing 40 mol % of cholesterol have been studied in the liquid-ordered phase at a microwave radiation frequency of 94 GHz. At such high field strengths, the spectra should be optimally sensitive to lateral chain ordering that is expected in the formation of in-plane domains. The high-field EPR spectra from random dispersions of the cholesterol-containing membranes display very little axial averaging of the nitroxide g-tensor anisotropy for lipids spin labeled toward the carboxyl end of the sn-2 chain (down to the 8-C atom). For these positions of labeling, anisotropic 14N-hyperfine splittings are resolved in the gzz and gyy regions of the nonaxial EPR spectra. For positions of labeling further down the lipid chain, toward the terminal methyl group, the axial averaging of the spectral features systematically increases and is complete at the 14-C atom position. Concomitantly, the time-averaged |
| Highly increased CSF concentrations of cholesterol precursors in Smith-Lemli-Opitz syndrome van Rooij, A., A. A. Nijenhuis, et al. (1997), J Inherit Metab Dis 20(4): 578-80. Abstract: The Smith-Lemli-Opitz syndrome is a genetic disorder characterized by typical clinical features including reduced myelination of both brain and peripheral nervous system and defective cholesterol biosynthesis. In patients this results in very low cholesterol concentrations and accumulation of cholesterol precursors in plasma, tissues, cultured cells and faeces. We now show that the cholesterol concentration in CSF of Smith-Lemli-Opitz patients is markedly decreased and that 7- and 8-dehydrocholesterol concentrations are highly increased in comparison to controls. Moreover, dietary treatment of patients with cholesterol seems not to affect CSF cholesterol concentration. |
| Highly purified scavenger receptor class B, type I reconstituted into phosphatidylcholine/cholesterol liposomes mediates high affinity high density lipoprotein binding and selective lipid uptake Liu, B. and M. Krieger (2002), J Biol Chem 277(37): 34125-35. Abstract: The murine class B, type I scavenger receptor mSR-BI is a high and low density lipoprotein (HDL and LDL) receptor that mediates selective uptake of cholesteryl esters. Here we describe a reconstituted phospholipid/cholesterol liposome assay of the binding and selective uptake activities of SR-BI derived from detergent-solubilized cells. The assay, employing lysates from epitope-tagged receptor (mSR-BI-t1)-expressing mammalian and insect cells, recapitulated many features of SR-BI activity in intact cells, including high affinity and saturable (125)I-HDL binding, selective lipid uptake from (3)Hcholesteryl ether-labeled HDL, and poor inhibition of HDL receptor activity by LDL. The novel properties of a mutated receptor (Q402R/Q418R, normal LDL binding but loss of most HDL binding) were reproduced in the assay, as was the ability of the SR-BI homologue CD36 to bind HDL but not mediate efficient lipid uptake. In this assay, essentially homogeneously pure mSR-BI-t1, prepared by single-step immunoaffinity chromatography, mediated high affinity HDL binding and efficient selective lipid uptake from HDL. Thus, SR-BI-mediated HDL binding and selective lipid uptake are intrinsic properties of the receptor that do not require the intervention of other proteins or specific cellular structures or compartments. |