Cholesterol Journal Articles

Record 8241 to 8260

Levels of total lipids, cholesterol and progesterone during estrus synchronization and pregnancy in sheep
Krajnicakova, M., E. Bekeova, et al. (1993), Vet Med (Praha) 38(6): 349-57.
Abstract: Our investigations were concerned with dynamic changes in total lipids (CL), cholesterol (CHOL) and progesterone (P4) in blood serum of sheep in the period of oestrus synchronization treatment and during mating and gravidity. Our experiment was carried out using 10 animals housed under the conditions of productive rearing. Blood samples were taken from v. jugularis on day of swab application (day 0) and on days 3 and 7 of the action of Agelin vaginal swabs, on day of insemination, and on days 7, 14, 17 and in the 2nd, 3rd and 4th month of gravidity. Blood serum was used to determine total lipids and cholesterol by means of Bio-Lachema tests, and P4 concentrations employing RIA-test-Prog kits (URVJT, Kosice). A statistically significant decrease in concentrations of total lipids (Fig. 1, Tab. I) in sheep blood serum was recorded on day of insemination (P < 0.05) compared to day 0, with the value 1.59 +/- 0.31 g/l of serum, and in the 3rd month of gravidity (P < 0.01), at concentrations 1.36 +/- 0.38 g/l of serum. The determined decrease in their values in the mentioned period can be modulated by the mutually changing ratio of steroid hormones or by inhibition of synthesis of lipoproteins responsible for changes in total plasma lipids. Changes in cholesterol concentrations (Fig. 2, Tab. I) during the introduction of swabs were insignificant and ranged from 1.60 +/- 0.42 to 1.73 +/- 0.33 mmol/l of serum. An insignificant increase in cholesterol concentrations (P < 0.05), with its highest levels 1.98 +/- 0.43 mmol/l of serum, was recorded in the 3rd month of gravidity.(ABSTRACT TRUNCATED AT 250 WORDS)

Leydig cell aging: steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage enzyme
Luo, L., H. Chen, et al. (2001), J Androl 22(1): 149-56.
Abstract: Primary points of control in steroidogenesis are the transport of cholesterol from intracellular stores to the inner mitochondrial membrane, and the subsequent conversion of cholesterol to pregnenolone by the cholesterol side-chain cleavage enzyme (P450scc). Testosterone production has been shown to decline in Brown Norway rat Leydig cells as the rats age. To better understand the mechanism by which aging Leydig cells lose steroidogenic function, we examined the effect of aging on steroidogenic acute regulatory protein (StAR), an important Leydig cell cholesterol transfer protein, and on P450scc. Leydig cells isolated from middle-aged (14 months) and old (24 months) rats produced significantly less testosterone than cells from young (4 months) rats. StAR mRNA (1.7 kilobase kb) was significantly reduced in Leydig cells from middle-aged and old rats, by 26% and 52%, respectively. Significant reductions also were seen in the steady-state levels of mRNA for P450scc, of 29% and 50%, respectively. Western blots revealed significant reductions in StAR protein, by 47% and 74%, respectively, and in P450scc protein, by 38% and 54%, respectively. In response to LH stimulation in vitro, testosterone production by Leydig cells in young, middle-aged, and old rats increased by 30-, 40-, and 33-fold, respectively, although the amounts of testosterone produced by the young cells significantly exceeded that produced by the middle-aged and old cells. StAR protein also increased in response to LH by 1.4-, 3-, and 11-fold, respectively, whereas P450scc protein remained unchanged. These results are consistent with the conclusion that compromise of StAR-mediated cholesterol transport may play a key role in age-related reductions in Leydig cell steroidogenesis. However, because P450scc is reduced in old Leydig cells, the reaction catalyzed by this enzyme would be rate-limiting under circumstances in which saturating amounts of cholesterol entered the mitochondria.

Liaison of apolipoprotein A with adipose cells: characteristics of the receptor sites and their role in the efflux of cholesterol
Barbaras, R., P. Puchois, et al. (1991), Journ Annu Diabetol Hotel Dieu: 39-43.

Library screening studies to investigate substrate specificity in the reaction catalyzed by cholesterol oxidase
Xiang, J. and N. S. Sampson (2004), Protein Eng Des Sel 17(4): 341-8.
Abstract: We tested whether it is possible to alter the substrate specificity of cholesterol oxidase for similarly sized sterols, i.e. cholesterol, beta-sitosterol and stigmasterol. Using existing X-ray crystal structures, we made a model of the predicted Michaelis complex of cholesterol and cholesterol oxidase. Based on this model, we identified five residues that are in direct contact with the steroid tail, Met58, Leu82, Val85, Met365 and Phe433. We prepared seven mutant libraries that contained the codon NYS (N = A, C, G, T; Y = C, Y; S = C, G) at one, two or three of the targeted positions by cassette mutagenesis. The libraries were screened for catalytic activity against three different sterols under k(cat)(*)/K(m)(*) conditions with 25 mol% sterol/DOPC unilamellar vesicles. The results of our screens suggest that specific packing interactions are not realized in the transition state of binding and that loss of active site water may be the predominant source of binding energy.

Librational motion of spin-labeled lipids in high-cholesterol containing membranes from echo-detected EPR spectra
Erilov, D. A., R. Bartucci, et al. (2004), Biophys J 87(6): 3873-81.
Abstract: Two-pulse, echo-detected (ED) electron paramagnetic resonance (EPR) spectroscopy was used to study the librational motions of spin-labeled lipids in membranes of dipalmitoylphosphatidylcholine + 50 mol % cholesterol. The temperature dependence, over the range 77-240 K, and the dependence on position of spin-labeling in the sn-2 chain (n=5, 7, 10, 12, and 14) of the phospholipid, were characterized in detail. The experimental ED-spectra were corrected for instantaneous spin diffusion arising from static spin-spin interactions, by using spectra recorded at 77 K, where motional contributions are negligible. Simulations according to a model of rapid, small-amplitude librations about an axis whose direction is randomly distributed are able to describe the experimental spectra. Calibrations, in terms of the amplitude-correlation time product, alpha2tauc, were constructed for diagnostic spectral line-height ratios at different echo delay times, and for relaxation spectra obtained from the ratio of ED-spectra recorded at two different echo delays. The librational amplitude, alpha2, was determined for a spin label at the 14-C position of the lipid chain from the partially motionally averaged hyperfine splitting in the conventional EPR spectra. The librational correlation time, tauc, which is deduced from combination of the conventional and ED-EPR results, lies in the subnanosecond regime and depends only weakly on temperature. The temperature dependence of the ED-EPR spectra arises mainly from an increase in librational amplitude with increasing temperature, and position down the lipid chain. A gradual transition takes place at higher temperatures, from a situation in which segmental torsional librations are cumulative, i.e., the contributions of the individual segments add up progressively upon going down the chain, to one of concerted motion only weakly dependent on chain position. Such librational motions are important for glass-like states and are generally relevant to high lipid packing densities, e.g., in cholesterol-containing raft domains and condensed complexes.

Libyan family with hypercholesterolemia and increased high-density lipoprotein cholesterol in plasma
Sheriff, D. S., M. el Fakhri, et al. (1994), Clin Chem 40(12): 2313-6.
Abstract: Genetic deficiencies of cholesteryl ester transport protein (CETP) and hepatic lipase activities have been associated with hyperalpha-lipoproteinemias. Here we present a family of 11 members, of which 9, including the father, mother, 5 sons, and 2 daughters, show a marked increase in high-density lipoprotein (HDL) cholesterol alone with low plasma concentrations of triglycerides. Analyses of lecithin:cholesterol acyltransferase (LCAT) activity, cholesteryl ester transfer between HDL fractions, hepatic lipase (HL) activity, and lipoprotein lipase (LPL) activity in these cases showed that a decrease in the heparin-releasable HL activity was the possible cause of the marked increase of HDL2 fractions observed in nine of them. Such a defect in HL activity could significantly affect HDL metabolism in particular and lipoprotein metabolism in general. Evidently, a marked increase in serum total cholesterol due to abnormal metabolism of HDL cholesterol, separate from known causes of altered low-density lipoprotein cholesterol metabolism, e.g., a clearance or a receptor defect, is not uncommon. The coordinated action of HL, LCAT, LPL, and CETP may be essential for normal metabolism of plasma lipoproteins.

Life style and cardiovascular risk factors in the Japanese population--from an epidemiological survey on serum lipid levels in Japan 1990 part 1: influence of life style and excess body weight on HDL-cholesterol and other lipid parameters in men
Yamamoto, A., H. Temba, et al. (2003), J Atheroscler Thromb 10(3): 165-75.
Abstract: Low HDL-cholesterol (HDL-C) has long been used as an important predictor of coronary artery disease (CAD), although HDL-C values themselves are influenced by various factors including serum triglyceride (TG) levels, obesity, and life style. In view of the importance of the metabolic syndrome as a risk factor of CAD, changes in HDL-C and other lipid parameters in the Japanese population associated with life style, especially in males, were analyzed in this study based on data obtained in an epidemiological survey carried out in 1990. Smokers had higher TG and lower HDL-C levels than non-smokers, while BMI and LDL-C were slightly decreased by smoking in middle-aged men (40-59 years old). Increases in both HDL-C and TG due to alcohol consumption were associated with an increase in BMI in younger men aged 20-39. In middle-aged men, significant increases in HDL-C were seen in every quintile of BMI, while the increase in TG levels due to alcohol was small. Middle-aged men engaged in occupations requiring greater physical activity also had higher HDL-C levels in every quintile of BMI. The influence of life style on serum lipid parameters appeared to be mostly expressed as a function of BMI in younger men, while it appeared to be independent of BMI in older men.

Life table methodology applied to NHANES II database for analysis of mortality associated with cholesterol/HDL ratios
Wesley, D. and D. Ingle (2001), J Insur Med 33(4): 310-5.
Abstract: This article describes the association between total cholesterol to high-density lipoprotein (HDL)-cholesterol ratios and all-cause mortality in a large cohort of Americans with nearly 17 years of follow-up. Detailed actuarial life table methodology was used. It concludes that the relationship is best described as a J-shaped curve.

Lifestyle determinants of HDL2- and HDL3-cholesterol levels in a hypercholesterolemic male population
Manttari, M., P. Koskinen, et al. (1991), Atherosclerosis 87(1): 1-8.
Abstract: In this cross-sectional study we investigated the role of lifestyle and other factors in determining serum HDL2- and HDL3-cholesterol levels among 82 dyslipidemic (total cholesterol minus HDL-cholesterol greater than or equal to 5.2 mmol/l) middle-aged participants of the Helsinki Heart Study. Alcohol consumption correlated positively with both subfractions of HDL-cholesterol, while leisure time physical activity had a significant correlation with the HDL3-subfraction only. HDL levels were lower in smokers than in non-smokers but the differences were not statistically significant. Using the multiple linear regression model, alcohol consumption emerged as the only significant factor influencing both HDL cholesterol subfraction levels. Leisure time physical activity had an independent contribution to HDL3-level, but lifestyle variables other than alcohol consumption did not contribute significantly to HDL2-cholesterol level. The model incorporating alcohol consumption, physical activity, smoking and relative body weight explained 13.4% of the variation in HDL2 and 17.5% in HDL3-cholesterol.

Lifestyle determinants of high-density lipoprotein cholesterol: the National Heart, Lung, and Blood Institute Family Heart Study
Ellison, R. C., Y. Zhang, et al. (2004), Am Heart J 147(3): 529-35.
Abstract: BACKGROUND: While genetic factors are major determinants of high-density lipoprotein cholesterol (HDL-C), environmental factors also play a role. The latter include 3 modifiable lifestyle factors: alcohol consumption, physical activity, and smoking. METHODS: We compared the relative effects of alcohol, physical activity, and smoking on HDL-C levels, using data from 2309 subjects (1226 women and 1083 men), aged 25 to 91 years, from randomly selected families participating in the National Heart, Lung, and Blood Institute Family Heart Study. RESULTS: Alcohol consumption was associated with the largest increment in HDL-C (an increase of 9.0-13.1 mg/dL from nondrinker to highest categories); physical activity with a more modest increment (an increase of 3.0-3.3 mg/dL from lowest to highest categories); and cigarette smoking with a large decrement in women (a decrease of 9.9 mg/dL) and a modest one in men (a decrease of 2.6 mg/dL) between nonsmoker and > or =20 cigarettes per day categories. The 3 lifestyle behaviors plus age, body mass index, education, and current estrogen use explained 22.4% and 18.2% of the total variance of HDL-C for women and men, respectively. Alcohol accounted for 28.6% of this variance among women and 50.1% among men; smoking accounted for 6.7% and 3.3%, respectively, and physical activity for 2.7% and 3.6%, respectively, among women and men. Age, body mass index, education, and current estrogen use explained the remaining 62.0% and 43.0%, respectively, of the variance attributed to environmental factors. CONCLUSIONS: This study suggests that, among lifestyle behaviors, alcohol consumption is the more important correlate of HDL-cholesterol.

Life-style factors do not explain racial differences in high-density lipoprotein cholesterol: the Minnesota Heart Survey
Sprafka, J. M., S. W. Norsted, et al. (1992), Epidemiology 3(2): 156-63.
Abstract: We analyzed data from a population-based survey to determine whether serum high-density lipoprotein cholesterol (HDL-C) concentrations are different in blacks and whites after controlling for life-style characteristics. We studied a total of 741 white men, 453 black men, 786 white women, and 572 black women age 35-74 years. Age-adjusted HDL-C concentrations were higher in black than white men (48.6 vs 40.8 mg/dl) and in black than white women (56.1 vs 54.0 mg/dl). Life-style characteristics associated with HDL-C in women were exogenous hormone use, average number of cigarettes smoked per day, average ounces of alcohol consumed per week, body mass index, and use of beta-blockers. Life-style characteristics associated with HDL-C levels in men included age, average number of cigarettes smoked per day, average ounces of alcohol consumed per week, body mass index, and a self-reported history of diabetes. After adjustment for life-style characteristics, black men and women had HDL-C levels 7.0 and 5.3 mg/dl higher, respectively, than whites. Body mass index was a negative confounder in women; after adjusting for body mass and age, black women had HDL-C levels 4.6 mg/dl higher than white women. These data indicate that the measured life-style factors cannot fully explain the observed differences in HDL-C between blacks and whites. These findings, which are consistent with other reports, may reflect an inability to assess life-style factors accurately and/or genetic or cultural factors yet to be determined.

Lifetime risk of coronary heart disease by cholesterol levels at selected ages
Lloyd-Jones, D. M., P. W. Wilson, et al. (2003), Arch Intern Med 163(16): 1966-72.
Abstract: BACKGROUND: We sought to assess how cholesterol levels at different ages modify the remaining lifetime risk of coronary heart disease (CHD). METHODS: We included all Framingham Heart Study participants examined from 1971 through 1996 who did not have CHD and were not receiving lipid-lowering therapy. At index ages of 40, 50, 60, 70, and 80 years, participants were stratified by total cholesterol level and by cholesterol subfractions. Lifetime risk of CHD was calculated with death free of CHD as a competing event. RESULTS: Among 3269 men and 4019 women, 1120 developed CHD and 1365 died free of CHD during follow-up. At each index age, lifetime risk of CHD increased with higher cholesterol levels, and time to event decreased. At age 40 years, the lifetime risks of CHD through age 80 years for men with total cholesterol levels less than 200 mg/dL (<5.20 mmol/L), 200 to 239 mg/dL (5.20-6.19 mmol/L), and 240 mg/dL or greater (> or =6.20 mmol/L), respectively, were 31%, 43%, and 57%; for women, the lifetime risks were 15%, 26%, and 33%, respectively. Lifetime risks contrasted sharply with shorter-term risks: at age 40 years, the 10-year cumulative risks of CHD were 3%, 5%, and 12% for men, and 1%, 2%, and 5% for women, respectively. CONCLUSIONS: Lifetime risk of CHD increases sharply with higher total cholesterol levels for men and women at all ages. These data support an important role for cholesterol screening in younger patients, and they may help target high-risk patients for lifestyle modification or drug therapy.

Ligand binding characteristics and aggregation behavior of purified cow's milk folate binding protein depends on the presence of amphiphatic substances including cholesterol, phospholipids, and synthetic detergents
Holm, J. and S. I. Hansen (2002), Biosci Rep 22(3-4): 431-41.
Abstract: Folate binding protein was purified from cow's milk by a combination of cation exchange chromatography and methotrexate-AH-sepharose affinity chromatography. Dilution of the preparation to concentrations of protein less than 10 nM resulted in drastic changes of radioligand (folate) binding characteristics, i.e., a decrease in binding affinity with a change from upward to downward convex Scatchard plots and increased ligand dissociation combined with appearance of weak-affinity aggregated forms of the binding protein on gel filtration. These findings, consistent with a model predicting dimerization between unliganded and liganded monomers, were reversed in the presence of material eluted from the affinity column after adsorption of the protein(cofactor) or cholesterol, phospholipids, and synthetic detergents. The latter amphiphatic substances form micelles and lipid bilayers which could separate hydrophobic unliganded monomers from hydrophilic liganded monomers in the surrounding aqueous medium and thereby prevent association between these monomeric forms prevailing at low concentrations of the protein. Our data have some bearings on studies which show that cholesterol and phospholipids are necessary for the clustering of folate receptors in the cell membrane; a process required for optimum receptor function and internalization of folate.

Ligand-activated pregnane X receptor interferes with HNF-4 signaling by targeting a common coactivator PGC-1alpha. Functional implications in hepatic cholesterol and glucose metabolism
Bhalla, S., C. Ozalp, et al. (2004), J Biol Chem 279(43): 45139-47.
Abstract: Previous studies show that feedback inhibition of bile acid production by bile acids is mediated by multiple mechanisms, including activation of pregnane X receptor (PXR). Consistent with these studies, the antibiotic rifampicin, a ligand for human PXR, reduces hepatic bile acid levels in cholestasis patients. To delineate the mechanisms underlying PXR-mediated suppression of bile acid biosynthesis, we examined the functional cross-talk between human PXR and HNF-4, a key hepatic activator of genes involved in bile acid biosynthesis including the cholesterol 7-alpha hydroxylase (CYP7A1) and sterol 12-alpha hydroxylase (CYP8B1) genes. Treatment with rifampicin resulted in repression of endogenous human CYP7A1 expression in HepG2 cells that was reversed by PXR small interfering RNA. The coactivator PGC-1 enhanced transcriptional activity of HNF-4, and this enhancement was suppressed by rifampicin-activated PXR. Endogenous PGC-1 from mouse liver extracts bound to PXR, and recombinant PGC-1 directly interacted with both PXR and HNF-4 in vitro. Rifampicin-dependent interaction of PXR with PGC-1 was shown in cells by coimmunoprecipitation, and intranuclear localization studies using confocal microscopy provided further evidence for this interaction. In chromatin immunoprecipitation studies, rifampicin treatment did not inhibit HNF-4 binding to the native promoters of CYP7A1 and CYP8B1 but resulted in dissociation of PGC-1 and concomitant gene repression. Most interestingly, these rifampicin effects were also observed in the phosphoenolpyruvate carboxykinase gene that contains a functional HNF-4-binding site and is central to hepatic gluconeogenesis. Our study suggests that ligand-activated PXR interferes with HNF-4 signaling by targeting the common coactivator PGC-1, which underlies physiologically relevant inhibitory cross-talk between drug metabolism and cholesterol/glucose metabolism.

Ligand-dependent contribution of RXRbeta to cholesterol homeostasis in Sertoli cells
Mascrez, B., N. B. Ghyselinck, et al. (2004), EMBO Rep 5(3): 285-90.
Abstract: We show that mice expressing retinoid X receptor beta (RXRbeta) impaired in its transcriptional activation function AF-2 (Rxrb(af20) mutation) do not display the spermatid release defects observed in RXRbeta-null mutants, indicating that the role of RXRbeta in spermatid release is ligand-independent. In contrast, like RXRbeta-null mutants, Rxrb(af20) mice accumulate cholesteryl esters in Sertoli cells (SCs) due to reduced ABCA1 transporter-mediated cholesterol efflux. We provide genetic and molecular evidence that cholesterol homeostasis in SCs does not require PPARalpha and beta, but depends upon the TIF2 coactivator and RXRbeta/LXRbeta heterodimers, in which RXRbeta AF-2 is transcriptionally active. Our results also indicate that RXRbeta may be activated by a ligand distinct from 9-cis retinoic acid.

Light and electron microscopic demonstration of cholesterol distribution in membrane structures of the rat auditory cortex
Dontchev, V., K. Ichev, et al. (1994), Acta Histochem 96(2): 165-74.
Abstract: As part of our investigations on the changes in the cortex of different stages of ontogeny, the aim of this study was to analyse the cholesterol distribution in the auditory cortex of adult rats. The light microscopic Schultz reaction as well as electron microscopic thin sections and freeze-etching combined with a cholesterol specific marker were applied to cholesterol demonstration. High and low cholesterol areas were found in the plasma membrane and membranes of some organelles. A low cholesterol content was observed in the membranes of the Golgi apparatus, mitochondria and junctional contacts. A very low cholesterol content was found in the pre- and postsynaptic membranes. High cholesterol contents were present in the neuronal and glial non-junctional plasma membranes. The cholesterol distribution in the membranes of the endoplasmic reticulum and nuclear envelope appeared to be different.

Limb malformations of rat fetuses exposed to a distal inhibitor of cholesterol biosynthesis
Chevy, F., F. Illien, et al. (2002), J Lipid Res 43(8): 1192-200.
Abstract: Triparanol, an inhibitor of desmosterol Delta24 reductase, produces a high rate of limb malformations in rat fetuses exposed at gestational day 10 (gd 10) to a single oral dose (150-200 mg/kg) given to the pregnant dam. AY9944, another efficient distal inhibitor of cholesterol biosynthesis that blocks dehydrocholesterol Delta7 reductase, produces a similar degree of cholesterol depletion but fewer malformations. Gas liquid chromatography-mass spectrometry (GC-MS) profiling of the sterols in the serum of the dams and in extracted embryos shows that in addition to desmosterol Delta24 reductase inhibition the conversion of Delta8 to Delta7 unsaturated sterols is also blocked by Triparanol. Therefore, the inhibitor induces the accumulation of desmosterol (Delta8 cholesten-3beta-ol, 8-dehydrocholesterol) and zymosterol (Delta8, Delta24 cholestadien-3beta-ol) in embryo tissues. The high concentration of the teratogenic drug assayed in the embryos at three successive gestational days (10-30 micro g/g) is thought to cause the blockade in both Delta24 reductase and Delta8-Delta7 isomerase, which results in the particular profile of aberrant sterols. Comparison of the animal model with human syndromes, including limb osseous and skeleton perturbations, suggests a combination of desmosterol and Delta8 unsaturated sterols as being involved in the deleterious influence on limb bone formation.

Limb, genital, CNS, and facial malformations result from gene/environment-induced cholesterol deficiency: further evidence for a link to sonic hedgehog
Lanoue, L., D. B. Dehart, et al. (1997), Am J Med Genet 73(1): 24-31.
Abstract: Low cholesterol levels produced by treating cholesterol deficient mutant mice with a cholesterol synthesis inhibitor (BM 15.766) between days 4 to 7 of pregnancy resulted in malformations consistent with those in the Smith-Lemli-Opitz syndrome (SLOS). Facial anomalies in mildly affected gestational day 12 mouse embryos included a small nose and long upper lip; in more severely affected embryos, the facial and forebrain anomalies are representative of holoprosencephaly. Additionally, abnormalities of the mid- and hind-brain were observed and included stenosis of the cerebral aqueduct at the level of the isthmus and apparent absence of the organ progenitor for the cerebellar vermis. Although not previously directly linked to cholesterol deficiency in experimental animals, limb and external genital defects were a notable outcome in this multifactorially-based cholesterol deficiency model. The results of this study provide new evidence supporting an important role for cholesterol in early embryonic development, provide additional support for the hypothesis that this role may involve the function of specific gene products, such as sonic hedgehog (shh) signaling protein, and provide a description of the pathogenesis of some of the characteristic malformations in SLOS.

Lime-treated maize husks lower plasma LDL-cholesterol levels in normal and hypercholesterolaemic adult men from northern Mexico
Vidal-Quintanar, R. L., R. L. Mendivil, et al. (1999), Br J Nutr 81(4): 281-8.
Abstract: Lime-treated maize husks (LTCH), a by-product of tortilla manufacturing in Mexico, have been shown to decrease plasma LDL-cholesterol levels in guinea-pigs by specific alterations in hepatic cholesterol metabolism. To determine whether LTCH would also lower plasma cholesterol levels in normal and hyperlipidaemic individuals, the fibre content of a typical diet was increased by supplementing free-living subjects in North-West Mexico with cookies containing 450 g LTCH/kg. Normal subjects (n 11) with plasma cholesterol levels of less than 5.7 mmol/l and hypercholesterolaemic subjects (n 12) with plasma cholesterol levels higher than 5.7 mmol/l participated in the study. Plasma glucose, cholesterol, triacylglycerol, LDL-cholesterol and HDL-cholesterol concentrations, LDL:HDL values and blood pressure were determined at baseline and after 6 weeks of supplementation with LTCH. LTCH supplementation significantly lowered the plasma total cholesterol level by 11-15% and LDL-cholesterol by 25%, and improved the LDL:HDL value by 29-33% (P < 0.01) in both normal and hypercholesterolaemic subjects. HDL-cholesterol, triacylglycerol and glucose concentrations did not change. Both groups consumed equal amounts of LTCH per week; individuals showed excellent compliance and good acceptance of the product. Neither group changed their dietary habits during the time of the experiment as determined by 3 d dietary records at baseline and at week 6. We conclude that LTCH supplements are suitable to increase fibre intake and reduce plasma LDL-cholesterol levels in healthy and hypercholesterolaemic subjects in this population.

Limitations of plasma plant sterols as indicators of cholesterol absorption
Vanstone, C. A. and P. J. Jones (2004), Am J Clin Nutr 79(2): 340-1.

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