| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Autoantibodies or immune defense against cholesterol? Horvath, I., E. Puskas, et al. (1994), Orv Hetil 135(18): 965-8. Abstract: Serological study was made on the lues aspecific positive sera (BAP); The serum reactivity was demonstrated by Kolmer and rapid plasma reagin (RPR) tests. The specificity was verified by treponema immobilization est (TPIT), fluorescent treponemal antibody (FTA-ABS) and treponema haemagglutination (TPHA) tests. The BAP sera were studied by enzyme labelled immunoassay (ELISA) with the isolated antigen components of Kolmer and RPR tests. The previously supposed "cardio-BAP" appeared only about 50 per cent of the sera. Anti-cholesterol antibody was demonstrated in 38 sera of 112 (33.9%) and only one of 50 negative control sera (2%). To the author's knowledge anti-cholesterol antibodies have never been demonstrated before. The authors suppose it is an autoantibody and their new result will give new possibilities to understand and explain the role of cholesterol in the so called "cholesterol diseases". Additional research have to be made to specify the pathological importance and role in the disorders. |
| Automated fluorimetric determination of cellular cholesterol Shahnaz, B., S. Tada, et al. (1998), Ann Clin Biochem 35 (Pt 5): 665-70. Abstract: We developed a completely automated fluorimetric method for the determination of cellular cholesterol, consisting of enzymatic hydrolysis of cholesteryl ester to free cholesterol and enzymatic oxidation of free cholesterol in the presence of an indicator substrate to produce a fluorescent product. For control preparations of monocytes, the mean detection limit was 2.57 mumol/5 x 10(5) cells and the mean within-batch coefficients of variation were 9.30, 6.00 and 3.73% at mean cholesterol concentrations of 1.94, 9.05 and 12.49 mumol/5 x 10(5) cells, respectively. The results correlated well with those obtained by gas-liquid chromatography. |
| Automated sample preparation for cholesterol determination in foods Johnson, J. H., P. McIntyre, et al. (1995), J Chromatogr A 718(2): 371-81. Abstract: An automated sample preparation system has been developed for the determination of cholesterol in a wide range of matrices. Isolation of cholesterol is performed with a robotic arm coupled with a series of modular stations. Samples are introduced into the system which adds the appropriate reagents, carries out the saponification, pH adjustment, solid-phase extraction and drying steps. This system was evaluated using 15 different food matrices. The average recovery for NIST standards exceeded 97%. A solution of n-hexane-2-propanol was substituted for the traditional methanol-chloroform extraction. Manual pH adjustment was replaced with a buffer. Manual and automated methods were compared and no difference was observed at the 95% confidence level. |
| Automatic gas chromatographic determination of the high-density-lipoprotein cholesterol and total cholesterol in serum Cardenas, M. S., E. Ballesteros, et al. (1995), J Chromatogr B Biomed Appl 672(1): 7-16. Abstract: A new analytical method that combines on-line precipitation-filtration, enzymatic hydrolysis, extraction and gas chromatography was developed for the determination of total cholesterol and high-density-lipoprotein cholesterol in human serum. Very-low-density lipoprotein, intermediate-density lipoprotein and low-density lipoprotein are precipitated with sodium phosphotungstate and magnesium chloride; then, the serum is continuously filtered and unprecipitated high-density-lipoprotein cholesterol is enzymatically hydrolyzed and finally determined as cholesterol by gas chromatography. Total cholesterol is also determined by direct introduction of the serum into the proposed system. The proposed method was validated by analyzing a lipid control serum with certified contents of high-density-lipoprotein cholesterol and total cholesterol. The results obtained were consistent with the certified contents. |
| Auto-oxidized cholesterol sulfates are antagonistic ligands of liver X receptors: implications for the development and treatment of atherosclerosis Song, C., R. A. Hiipakka, et al. (2001), Steroids 66(6): 473-9. Abstract: Liver X receptors (LXRs) are members of the nuclear receptor superfamily that are involved in regulation of cholesterol transport and metabolism. Expression of cholesterol 7alpha-hydroxylase, cholesteryl ester transfer protein and certain ATP-binding cassette transporters that are responsible for cholesterol efflux from cells is regulated by LXR and its ligands. In this report we show that 5alpha, 6alpha-epoxycholesterol-3-sulfate (ECHS) and 7-ketocholesterol-3-sulfate inhibit transactivation of a reporter gene by LXR. Non-sulfated forms of these compounds, as well as many other steroid sulfates, had no antagonistic activity. Using chimeric receptors, the antagonistic activity of ECHS was dependent on its interaction with the ligand-binding domain of LXR. ECHS disrupts recruitment of the co-activator Grip 1 into a complex with agonist-bound LXR and this may be responsible for the observed antagonistic properties of these compounds. In various cultured cells, these LXR antagonists also promote de novo cholesterol synthesis and apoptosis. 7-Ketocholesterol and 5alpha, 6alpha-epoxycholesterol are present in blood and have been found in atherosclerotic plaques. If sulfated forms of these oxidized sterols are also present, they may have an important role in foam cell formation by inhibiting LXR function. Since LXR agonists can counteract the activity of these antagonists, they may have therapeutic potential against atherosclerosis. |
| Autosomal recessive hypercholesterolaemia: normalization of plasma LDL cholesterol by ezetimibe in combination with statin treatment Lind, S., A. G. Olsson, et al. (2004), J Intern Med 256(5): 406-12. Abstract: BACKGROUND: Severe hereditary hypercholesterolaemia is most frequently due to familial hypercholesterolaemia (FH), caused by mutations in the LDL receptor (LDLR) gene. However, a phenotype very similar to FH may also be caused by defects in other genes like the genes for apolipoprotein (apo) B-100 or autosomal recessive hypercholesterolaemia (ARH). SUBJECT: An 8-year-old male of Lebanese origin was diagnosed with severe hypercholesterolaemia and extensive cutaneous and tendon xanthomas. Plasma LDL cholesterol before treatment was 17 mmol L(-1), whilst parents and both siblings had normal levels. DIAGNOSIS: Degradation of (125)I-labelled LDL in blood lymphocytes was reduced, but not abolished. Sequencing analysis of the LDLR and apoB-100 genes were negative, whilst a splice acceptor mutation in intron 1 (IVS 1 -1G>C) was detected in the ARH gene. The patient was homozygous for the mutation, whilst the parents were heterozygous. These findings were in agreement with a diagnosis of ARH. TREATMENT AND CLINICAL COURSE: Monthly LDL apheresis and atorvastatin 120 mg daily reduced LDL cholesterol preapheresis level to 4.8 mmol L(-1). When ezetimibe was given 10 mg day(-1) in combination with rosuvastatin 80 mg day(-1), LDL cholesterol was further lowered to 1.6 mmol L(-1), which made apheresis unnecessary. Cutaneous and tendon xanthomas disappeared completely and the intima-media thickness of the common carotid arteries decreased. At age 23 he developed a small myocardial infarction. CONCLUSION: ARH should be considered in cases of severe hypercholesterolaemia with a pattern of recessive inheritance. Combination therapy with high-dose statin and ezetimibe seems to be the treatment of choice in ARH and may reduce or eliminate the need for LDL apheresis treatment. |
| Availability for enzyme-catalyzed oxidation of cholesterol in mixed monolayers containing both phosphatidylcholine and sphingomyelin Mattjus, P. and J. P. Slotte (1994), Chem Phys Lipids 71(1): 73-81. Abstract: In this study we have examined the interaction between cholesterol and phospholipids in monolayers using cholesterol oxidase (Streptomyces cinnamomeus) as a probe. Monolayers containing cholesterol and phospholipids in different molar ratios were exposed to cholesterol oxidase at a lateral surface pressure of 20 mN/m (at 30 degrees C). The rate of cholesterol oxidation by cholesterol oxidase was faster in a monolayer consisting of a mono-unsaturated phospholipid (either 1-stearoyl-2-oleoyl-sn-glycero-3-phosphocholine (SOPC) or N-oleoyl-sphingomyelin (O-SPM)) and cholesterol than it was in a monolayer of a saturated phospholipid (either 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) or N-stearoyl-sphingomyelin (S-SPM)) and cholesterol. This suggests that the susceptibility of cholesterol to oxidation by cholesterol oxidase was markedly affected by the phospholipid acyl chain composition. In addition, cholesterol was oxidized more readily in a phosphatidylcholine-containing monolayer as compared with a sphingomyelin monolayer (at a similar degree of acyl chain saturation). The average rate of oxidation, as a function of the cholesterol/phospholipid (C/PL) molar ratio in a binary monolayer (with cholesterol and one phospholipid class), was linear except for one discontinuity, at 1:1 for phosphatidylcholine monolayers (either SOPC or DSPC) and at 2:1 for sphingomyelin monolayers (O-SPM or S-SPM). We interpret these discontinuities as indicating the stoichiometry at which cholesterol can exist dispersed in the monolayer without lateral segregation into cholesterol-rich clusters. Next, ternary monolayers were examined (with cholesterol and one phosphatidylcholine and one sphingomyelin species).(ABSTRACT TRUNCATED AT 250 WORDS) |
| Awareness and use of blood cholesterol tests in 40-74-year-olds by educational level Polednak, A. P. (1992), Public Health Rep 107(3): 345-51. Abstract: Questions on awareness, use, and results of blood cholesterol tests were included in telephone surveys on cancer conducted in 1988 on random samples of persons 40-74 years of age in Long Island, NY (N = 440), and in Connecticut (N = 453). Educational level was significantly and positively associated with the proportions reporting ever having heard of blood cholesterol tests, ever having had a test done ("by a doctor"), and having a recent test, 1987-88, but not with the proportion reportedly having been told by a doctor that their cholesterol level was "high." In multivariate analyses, greater education (college graduate versus all others) and greater frequency of medical checkups (annual versus other) were significant independent predictors of ever having had a cholesterol test or having been tested in 1987 or 1988. Implications of findings were discussed with regard to monitoring changes over time in awareness and use of cholesterol tests according to educational level and to planning interventions aimed at less educated groups. |
| Awareness of cholesterol as coronary risk factor among general practitioners at Jaipur Gupta, R., B. K. Jain, et al. (1993), J Assoc Physicians India 41(11): 717-9. Abstract: Widespread information about preventive measures has decreased incidence of coronary artery disease (CAD) in developing countries. However this trend is not seen in India. Cholesterol and other lipoproteins play important role in CAD. In order to assess whether this information has reached General Practitioners (GP's) and their action regarding the recommendations of the US National Cholesterol Education Programme (NCEP), G.P.'s were assessed with the help of a questionnaire. The response rate to the questionnaire was 78.4% of the total G.P.'s of the city. The findings of the study were compared to the NCEP guidelines. Results indicate that, "Ideal", "High" and cholesterol levels dietary needing precautionary measures intervention (ie. 198.2 +/- 13 mg/dl, 256.1 +/- 32 mg/dl and 247.9 +/- 26 mg/dl respectively) were similar to the NCEP guidelines. Levels where therapy is recommended (ie 293.9 +/- 34 mg/dl) is significantly more than NCEP guidelines. Though 77.1% of doctors were aware of protective effect of HDL cholesterol (ie 51.1 +/- 6 mg/dl), routine measurement of lipid profile was undertaken by only 57.1% doctors with mean age of recommendation being 34.1 +/- 11.6. Routine dietary advice and cholesterol estimation was done in 71.4% patients with CAD and 67.3% of patients with hypertension and diabetes. Analysis of action taken falls short of the NCEP recommendations and indicates a need for intensive training of the G.P.s. |
| Axonal regeneration, but not myelination, is partially dependent on local cholesterol reutilization in regenerating nerve Goodrum, J. F., J. C. Brown, et al. (2000), J Neuropathol Exp Neurol 59(11): 1002-10. Abstract: A recycling pathway in peripheral nerve permits cholesterol from degenerating myelin to be salvaged by macrophages and resupplied to myelinating Schwann cells by locally produced lipoproteins. A similar reutilization of cholesterol by regenerating axons has been proposed but not demonstrated. Neurites in culture, however, do take up cholesterol and cholesterol-containing lipoproteins, where these molecules are found to promote neurite extension. To test the requirement for cholesterol reutilization in axon regeneration and myelination, we examined 2 models of blocked intracellular cholesterol transport: 1) bone marrow transplants from Niemann-Pick C mice into wild-type recipient mice, and 2) imipramine treatment. Following nerve crush in these models, we found that unusually large, debris-filled macrophages appeared and persisted for many weeks. A morphometric analysis of regenerating nerves revealed that myelination proceeded at a normal rate (normal g-ratios), but that axon growth was retarded (decreased fiber numbers and diameters) in these animals. Cholesterol synthesis was elevated in these nerves, indicating that Schwann cells compensated for the decreased exogenous supply of cholesterol by up-regulating de novo synthesis to support myelination. These data indicate that Schwann cells are not dependent on cholesterol reutilization to support myelination, but that optimal axonal regeneration is dependent on a local supply of cholesterol. |
| Axon-dominant localization of cell-surface cholesterol in cultured hippocampal neurons and its disappearance in Niemann-Pick type C model cells Tashiro, Y., T. Yamazaki, et al. (2004), Eur J Neurosci 20(8): 2015-21. Abstract: There is growing evidence showing the important role of cholesterol in maintaining neuronal function. In particular, much attention has been paid to the role of the cholesterol-rich microdomains called lipid rafts. However, the cholesterol distribution on neurons is not clear. Here, we investigated localization of cholesterol in cultured rat hippocampal neurons, using filipin and a novel cholesterol-binding reagent BCtheta. In our culture system, BCtheta detects only cell-surface cholesterol, whereas filipin stains both intracellular and cell-surface cholesterol. BCtheta staining appeared visible in a maturation-dependent manner and showed axon-dominant distribution of cell-surface cholesterol in fully matured neurons. A part of this cholesterol on axons was resistant to detergents at 4 degrees C, and thus might be involved in lipid rafts. Interestingly, Niemann-Pick type C model neurons induced by class 2 amphiphiles lost the cell-surface but not the intracellular cholesterol staining. Niemann-Pick type C disease is caused by the disruption of intracellular cholesterol transport and is known to induce neurodegeneration in brains accompanied by formation of neurofibrillary tangles. Our observations suggest the important role of cell-surface cholesterol in maintaining a functional axonal membrane and indicate that the observed defect in axonal surface cholesterol might lead to neurodegeneration. |
| Azalanstat (RS-21607), a lanosterol 14 alpha-demethylase inhibitor with cholesterol-lowering activity Burton, P. M., D. C. Swinney, et al. (1995), Biochem Pharmacol 50(4): 529-44. Abstract: Agents that inhibit hepatic cholesterol biosynthesis reduce circulating cholesterol levels in experimental animals and humans, and may be of pharmacological importance in the prevention of atherosclerosis. Azalanstat (RS-21607), a synthetic imidazole, has been shown to inhibit cholesterol synthesis in HepG2 cells, human fibroblasts, hamster hepatocytes and hamster liver, by inhibiting the cytochrome P450 enzyme lanosterol 14 alpha-demethylase. When administered orally to hamsters fed regular chow, RS-21607 (50 mg/kg/day) lowered serum cholesterol in a dose-dependent manner (ED50 = 62 mg/kg) in a period of 1 week. It preferentially lowered low density lipoprotein (LDL) cholesterol and apo B relative to high density lipoprotein (HDL) cholesterol and apo A-1. It also lowered plasma cholesterol levels in hamsters fed a high saturated fat and cholesterol diet. RS-21607 inhibited hepatic microsomal hydroxymethylglutaryl-CoA (HMG-CoA) reductase activity in hamsters in a dose-dependent manner (ED50 = 31 mg/kg), and this was highly correlated with serum cholesterol lowering (r = 0.97). Cholesterol lowering by azalanstat and cholestyramine was additive, and the increase in HMG-CoA reductase brought about by cholestyramine was attenuated significantly by azalanstat. In vitro studies with HepG2 cells indicated that this modulation of reductase activity was indirect, occurring at a post-transcriptional step, and it is proposed that a regulatory oxysterol derived from dihydrolanosterol (or lanosterol) may be responsible for this regulation. Azalanstat does not appear to lower circulating cholesterol in the hamster by up-regulation of the hepatic LDL receptor, suggesting that other mechanisms are involved. Orally administered azalanstat (50-75 mg/kg) stimulated hepatic microsomal cholesterol 7 alpha-hydroxylase activity by 50-400% in hamsters, and it is postulated that this may result from modified cholesterol absorption and bile acid synthesis. |
| Back to basics. Cholesterol Roberts, S. S. (2005), Diabetes Forecast 58(3): 33-5. |
| Bacteria and cholesterol gallstones: molecular biology comes to gallstone pathogenesis Soloway, R. D. and R. S. Crowther (1995), Gastroenterology 108(3): 934-6. |
| Bacteria-host cell interaction mediated by cellular cholesterol/glycolipid-enriched microdomains Shin, J. S., Z. Gao, et al. (1999), Biosci Rep 19(5): 421-32. Abstract: Gram negative bacterial infection is a leading cause of fatality and is attributed, at least in part, to the bacteria's capacity to persist in the host in spite of appropriate antibiotic therapy. It has been suggested that bacteria evade antibiotics by hiding within host cells. We sought to investigate this important aspect of infections in mast cells, which are inflammatory cells found in close proximity to the host-environment interface and which have recently been reported to play a crucial role in the early innate immune response to bacteria. We examined mast cell interactions with FimH-expressing E. coli, one of the major opportunistic pathogens of humans. We determined that in serum free conditions, these bacteria were able to trigger mast cell uptake without loss of bacterial viability. CD48, a mannose containing GPI (glycosylphosphatidylinositol)-linked molecule was found to be the receptor of FimH-expressing E. coli in mouse mast cells. We found that the internalization via CD48 was blocked by filipin, a cholesterol binding drug known to disrupt cholesterol/glycolipid-enriched microdomains and the bacteria-encasing vacuoles were rich in cholesterol inside cells. Interestingly, we found that mast cells subsequently expelled majority of the intracellular bacteria in 24 hours. This expulsion process was blocked by lovastatin/cyclodextrin treatment, which is known to inhibit cellular trafficking of cholesterol/glycolipid-enriched microdomains. Thus, the bacterial entry into and expulsion from mast cells were critically dependent on cholesterol/glycolipid-enriched microdomains, which represents a novel mode of tussle between the pathogen and the mast cell occurring in opsonin deficient sites in the body or even at other sites in naive or immunocompromised hosts which have low systemic levels of E. coli specific antibody. |
| Bacterial cholesterol oxidases are able to act as flavoprotein-linked ketosteroid monooxygenases that catalyse the hydroxylation of cholesterol to 4-cholesten-6-ol-3-one Molnar, I., N. Hayashi, et al. (1993), Mol Microbiol 7(3): 419-28. Abstract: A new metabolite of cholesterol was found in reaction mixtures containing cholesterol or 4-cholesten-3-one as a substrate and extra- or intracellular protein extracts from recombinant Streptomyces lividans and Escherichia coli strains carrying cloned DNA fragments of Streptomyces sp. SA-COO, the producer of Streptomyces cholesterol oxidase. The new metabolite was identified as 4-cholesten-6-ol-3-one based on comparisons of its high-performance liquid chromatography, gas chromatography/mass spectrometry, infrared and proton-nuclear magnetic resonance spectra with those of an authentic standard. Genetic analyses showed that the enzyme responsible for the production of 4-cholesten-6-ol-3-one is cholesterol oxidase encoded by the choA gene. Commercially purified cholesterol oxidase (EC 1.1.3.6.) of a Streptomyces sp., as well as of Brevibacterium sterolicum and a Pseudomonas sp., and a highly purified recombinant Streptomyces cholesterol oxidase were also able to catalyse the 6-hydroxylation reaction. Hydrogen peroxide accumulating in the reaction mixtures as a consequence of the 3 beta-hydroxysteroid oxidase activity of the enzyme was shown to have no role in the formation of the 6-hydroxylated derivative. We propose a possible scheme of a branched reaction pathway for the concurrent formation of 4-cholesten-3-one and 4-cholesten-6-ol-3-one by cholesterol oxidase, and the observed differences in the rate of formation of the 6-hydroxy-ketosteroid by the enzymes of different bacterial sources are also discussed. |
| Bafilomycin A1, a specific inhibitor of vacuolar-type H(+)-ATPase, blocks lysosomal cholesterol trafficking in macrophages Furuchi, T., K. Aikawa, et al. (1993), J Biol Chem 268(36): 27345-8. Abstract: Certain steroids having an oxo group at the C-17 or C-20 position such as pregnenolone and dehydroisoandrosterone inhibit the cholesterol transport from lysosomes to other cellular sites. Taking advantage of the fact that the inhibition is reversed upon removal of the steroids, we studied the factors that control the cholesterol transport from lysosomes to other cellular sites in macrophages. Macrophages that accumulated unesterified cholesterol in their lysosomes were prepared by incubating cells with liposomes containing cholesterol and phosphatidylserine in the presence of a steroid inhibitor. These cells were chased by means of steroid washout, and then the effects of various pharmacological agents on the subsequent metabolism of cholesterol were examined. When the cells were chased in the absence of the agents, some of the cholesterol was converted to cholesteryl esters in the cells, and others were desorbed into the medium as unesterified forms, suggesting recovery of lysosomal cholesterol trafficking. Among the agents tested, bafilomycin A1, a specific inhibitor of vacuolar-type H(+)-ATPase, completely blocked both cholesterol esterification and cholesterol desorption at 10 nM. Moreover, agents that neutralize the lysosomal proton gradient, such as ammonium chloride and chloroquine, also reduced both of the processes. Fluorescent microscopic examination of bafilomycin A1-treated cells revealed extensive filipin-cholesterol staining of perinuclear lysosomes. From these data, we conclude that acidic pH is required for the efflux of cholesterol from lysosomes to other cellular sites. |
| Baked rye products modify cholesterol metabolism and crypt cell proliferation rates in rats Lund, E. K., K. L. Salf, et al. (1993), J Nutr 123(11): 1834-43. Abstract: Young adult male rats were made hypercholesterolemic by feeding cholesterol (+ cholic acid). The effect of rye crispbread on hepatic and plasma cholesterol concentrations, hepatic cholesterol synthesis, small intestinal cell turnover and fecal output was investigated. Diets containing 50 and 75% rye crispbread (g dry wt) were compared with positive control diets of similar gross composition, in which the insoluble component of rye was matched with cellulose and the soluble component with guar gum. A negative control diet containing no non-starch polysaccharide was also included. Cholesterol supplementation was maintained in half the rats on each diet. Rye caused a marked increase in fecal output that was greater than that seen in the positive control groups. However, crypt cell proliferation in the small intestine was less than that seen in the high fiber control groups. Rye reduced total plasma cholesterol concentrations only in those rats that continued to receive the high cholesterol diet. However, whether or not cholesterol was fed, the presence of nonstarch polysaccharide caused a decrease in liver cholesterol concentrations. Rye caused a marked increase in hepatic cholesterol synthesis over both the positive controls and the rats fed a fiber-free diet. This implies that rye causes a loss of cholesterol from the body, probably due to malabsorption of bile acids and cholesterol. |
| Bakery products enriched with phytosterol esters, alpha-tocopherol and beta-carotene decrease plasma LDL-cholesterol and maintain plasma beta-carotene concentrations in normocholesterolemic men and women Quilez, J., M. Rafecas, et al. (2003), J Nutr 133(10): 3103-9. Abstract: The hypocholesterolemic effects of phytosterols have not been evaluated in bakery products, and the addition of liposoluble antioxidants to the carrier has never been tested. We investigated the effects of consuming croissants and magdalenas (Spanish muffins) enriched with sterol esters, alpha-tocopherol and beta-carotene on plasma lipid and fat-soluble antioxidant concentrations in normocholesterolemic, habitual consumers of bakery products following their usual diet and lifestyle. Using a randomized, double-blind, placebo-controlled design, the control (C) group (n = 29) received two pieces daily (standard croissant and muffin) and the sterol ester (SE) group (n = 28), the same products with sterol esters added (3.2 g/d) for 8 wk. Total and LDL cholesterol (LDL-C) decreased in the SE group by 0.24 mmol/L (P < 0.01) and 0.26 mmol/L (P < 0.005), respectively, whereas these variables did not change in the control group. The total difference in total and LDL-C changes between groups was 0.38 mmol/L (8.9%) and 0.36 mmol/L (14.7%), respectively (P < 0.001). Within-group changes in HDL cholesterol, triacylglycerol or lipoprotein(a) concentrations did not differ. Similarly, within-group changes over time in plasma tocopherol and carotenoid concentrations did not differ between groups. Our findings suggest that bakery products are excellent carriers for phytosterols, and their consumption is associated with a decrease in total and LDL-C concentrations, with no changes in alpha-tocopherol and beta-carotene. The ability of bakery products to include sufficient quantities of beta-carotene to compensate for a potential deficiency, and the fact that their efficacy was not associated with the time of day at which they were consumed, are interesting findings. |
| Bakery products lower serum cholesterol concentrations in hypercholesterolemic men Anderson, J. W., S. Riddell-Lawrence, et al. (1991), Am J Clin Nutr 54(5): 836-40. Abstract: Several foods rich in water-soluble fiber have documented hypocholesterolemic effects. To determine the cholesterol-lowering effects of high-soluble-fiber intake from refined, wheat-based bakery products, 10 hypercholesterolemic subjects ate a high-carbohydrate, high-fiber control diet in a metabolic ward for 7 d, followed by a diet rich in soluble fiber from bakery products for 21 d. Both control and bakery diets provided 25 g total dietary fiber/d; however, the bakery diet provided 6 g soluble fiber/d more than the control diet. Average serum total cholesterol concentrations stabilized during the control diet and then decreased 6.4% during the bakery diet. Serum low-density-lipoprotein cholesterol decreased 8.5% (P less than 0.05), apolipoprotein B-100 decreased 8.7% (P less than 0.05), and the ratio of apolipoprotein B-100 to apolipoprotein A-I decreased 9.5% (P less than 0.05) during the bakery diet. Results confirm previous reports that a small increase in soluble-fiber intake of approximately 6 g/d modestly decreases atherogenic serum cholesterol concentrations, regardless of fiber source. |