| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Physical partitioning is the main mechanism of alpha-tocopherol and cholesterol transfer between lipoproteins and P388D1 macrophage-like cells Asmis, R. (1997), Eur J Biochem 250(2): 600-7. Abstract: The regulation of cellular vitamin E concentration was studied in P388D1 macrophage-like cells. Cellular alpha-tocopherol levels increased more than 5000-fold over constitutive levels without reaching saturation when P388D1 cells were cultured in vitamin-E-supplemented fetal calf serum. The uptake of alpha-tocopherol was accompanied by accumulation of alpha-3Htocopherol and 14Ccholesterol in these cells. Human unmodified low-density lipoprotein (LDL) inhibited the uptake of alpha-3Htocopherol and 14Ccholesterol in a dose-dependent manner and with very similar IC50. Acetylated, Cu2+-oxidized and aggregated human LDL and human very-low-density-lipoprotein (VLDL) were similarly potent, whereas human HDL was at least tenfold less effective than human LDL when inhibitory activity was correlated to lipoprotein protein levels. The rate of vitamin E uptake by P388D1 cells, however, always correlated with the extracellular alpha-tocopherol/cholesterol ratio. Efflux of alpha-3Htocopherol from labeled P388D1 cells required extracellular acceptors and was accompanied by the concomitant release of 14Ccholesterol. Both human LDL and HDL could serve as acceptors. Changes in the cellular alpha-tocopherol level appear to be the direct consequence of changes in the extracellular alpha-tocopherol/cholesterol ratio due to a rapid exchange of lipids between P388D1 cells and their extracellular environment. While the transfer of alpha-tocopherol from LDL, VLDL, and fetal calf serum into P388D1 cells appears to occur mainly by diffusion, HDL-stimulated efflux of alpha-tocopherol may underlie a different mechanism. The alpha-tocopherol/cholesterol ratio of the extracellular environment may be a critical factor in determining cellular vitamin E levels in vivo. |
| Physician follow-up of a community cholesterol-screening project Kass, D. and J. Hickner (1991), Fam Pract Res J 11(2): 139-48. Abstract: We report the results of physician follow-up of a group of community cholesterol-screening participants with hypercholesterolemia two years after the initial screening. Of 443 participants in a 1987 screening program, 51 (12%) had a cholesterol greater than the program cutoff of 7.16 mmol/L (277 mg/dL). In 1989, follow-up data from office records review and patient questionnaires were available on 48 (94%) of the 51 participants. Forty-three participants (90%) had consulted with a physician as advised. Twenty-five participants (66%) of the charts reviewed) had lipid profiles performed subsequent to the 1987 screening. Of the 43 participants consulting their physicians, twenty-six (60%) were prescribed a lipid-lowering regimen. Twenty-two were prescribed diet alone, fourteen also received prescriptions for medication, and two were advised to exercise more. Thirty subjects had had cholesterol levels checked in 1989, two years after the screening program. This group experienced an average decrease of 1.32 mmol/L (51 mg/dL), but several confounding factors may have contributed to this 16%-mean decline in cholesterol. Men were underrepresented throughout the screening and follow-up process. This community cholesterol-screening project in a small rural community achieved a high physician follow-up rate. |
| Physicians and cholesterol Faergeman, O. (1990), Ugeskr Laeger 152(20): 1461. |
| Physicians' attitudes to the treatment of elevated serum cholesterol McDermid, G., C. C. Lang, et al. (1990), J R Coll Physicians Lond 24(4): 271-6. Abstract: A questionnaire was sent to 457 physicians (328 general practitioners, 129 hospital doctors) to assess their attitudes to and their knowledge and practice of the management of raised serum cholesterol. Replies were returned by 206 (63%) general practitioners and 95 (74%) hospital doctors. While smoking, hypertension, diabetes mellitus and elevated total serum cholesterol were recognised as major risk factors for coronary heart disease, a significant number of respondents considered serum triglycerides to be less important. Both groups of physicians start dietary management at similar total serum cholesterol levels, but hospital doctors were more likely to use dietetic services. The two groups had a similar threshold for the addition of drug therapy. A bile acid sequestrant was the favoured first choice as a cholesterol lowering agent, although a wide variety of other drugs were also chosen. The screening of high risk patients was preferred to whole population and opportunistic screening for identifying hypercholesterolaemic individuals. The findings have important implications in the delivery of services to hypercholesterolaemic patients. |
| Physicians' perspectives on cholesterol and heart disease O'Keefe, C. E., D. F. Hahn, et al. (1991), J Am Diet Assoc 91(2): 189-92. Abstract: In early spring of 1988, questionnaires were mailed to 4,000 Midwestern physicians to survey their attitudes and practices regarding elevated serum cholesterol and their use of referrals for nutrition counseling; 633 physicians responded. Sixty-eight percent of the physicians thought that reducing high serum cholesterol levels would substantially affect heart disease; however, physicians attributed considerably less preventive value to reducing the cholesterol level than to reducing blood pressure (80.3%) or ceasing smoking (90.0%). The range of serum cholesterol for which diet therapy was most frequently initiated was 5.70 to 6.20 mmol/L. The most frequent range for initiation of drug therapy was 7.80 to 8.25 mmol/L. The physicians reported that although their medical school training did not prepare them adequately for providing diet counseling, they did feel prepared to provide, and were successful in, counseling on diet modifications for reducing serum cholesterol. Few (10%) of the total sample reported having registered dietitians available for dietary counseling, and most (88.8%) believed that it is the physician's responsibility to provide such counseling. Although the low response rate limits the conclusions of the survey, it is likely that those physicians most interested in the topic responded. We conclude that registered dietitians should explore the need for their special services further. More aggressive marketing of dietetic services could benefit both physicians and patients in the campaign to reduce serum cholesterol. |
| Physicochemical changes in human high-density lipoproteins (HDL) oxidized by gamma radiolysis-generated oxyradicals. Effect on their cholesterol effluxing capacity Bonnefont-Rousselot, D., C. Motta, et al. (1995), Biochim Biophys Acta 1255(1): 23-30. Abstract: This paper describes an oxidative process of human high-density lipoproteins (HDL) based upon the action of oxygenated free radicals produced by water radiolysis (OH. and OH./O2.- free radicals at pH 7), monitored by both biochemical and physical markers. Classical biochemical markers (vitamin E, thiobarbituric acid-reactive substances (TBARS), conjugated dienes and differential fluorescence) were studied as a function of the radiation dose (from 0 to 800 Gy; dose rate = 2.7 x 10(-2) Gy.s(-1)). The fluorescence polarization anisotropy (r) was measured with 1,6-diphenylhexatriene (DPH). Vitamin E decrease and formation of lipid peroxidation products (thiobarbituric acid-reactive substances and conjugated dienes) were concomitant in the case of OH. free radicals alone, whereas these products appeared after a small threshold dose when OH. and O2.- free radicals were simultaneously produced in solution. At high radiation doses, TBARS concentrations have reached plateau values (approx. 2 or 7 nmol/mg lipid with OH. or OH./O2.- free radicals, respectively) which were much lower than those obtained after copper oxidation (approx. 15 or 29 nmol/mg lipid after 12 and 24 h incubation, respectively). The free radical-induced oxidative process has led to a rigidification of the HDL and was associated with low values of cholesterol effluxing capacities when these oxidized HDL were incubated with cholesterol-loaded human fibroblasts. Similar results were obtained with copper-oxidized HDL, under our experimental conditions. Consequently, these two kinds of oxidative modification of HDL resulted both in a loss of their capacity to remove cellular cholesterol, which could be explained by the fact that this ability was under the dependence of a HDL optimum fluidity. |
| Physiologic mechanisms for reduced apolipoprotein A-I concentrations associated with low levels of high density lipoprotein cholesterol in patients with normal plasma lipids Gylling, H., G. L. Vega, et al. (1992), J Lipid Res 33(10): 1527-39. Abstract: Low plasma concentrations of high density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apoA-I) are major risk factors for coronary heart disease (CHD). Low HDL levels are common in patients with hypertriglyceridemia, but they also occur in those with normal plasma lipids; the latter include obese patients and cigarette smokers, though other patients with low HDL levels are neither obese nor smokers. The present study was designed to define metabolic causes of low apoA-I levels in normal-weight, normolipidemic patients. ApoA-I tracer studies were carried out in two groups of normolipidemic patients having low HDL levels to determine input rates and residence times for ApoA-I; these patients included 11 nonobese nonsmokers and 11 nonobese cigarette smokers. Their results were compared to those of 20 normal-weight, normolipidemic controls with normal HDL levels and 12 obese nonsmokers also having low HDL. In all three groups manifesting low HDL-cholesterol and low apoA-I levels, residence times for plasma apoA-I were reduced by approximately 30%, compared to control subjects with normal HDL levels. In contrast, average input rates for apoA-I were similar among the three low-HDL patients and control subjects. No differences in apoA-I kinetics were observed among any of the three groups with low apoA-I concentrations. Within each of the four groups of the study, however, input rates for apoA-I were highly correlated with plasma concentrations of apoA-I. Thus, for individuals with normal levels of plasma lipids, both residence times and input rates for apoA-I appeared to be important determinants of apoA-I levels. Residence times for apoA-I were reduced in almost all patients with low apoA-I levels, regardless of concomitant factors, whereas input rates were highly variable among individuals. |
| Physiologic role and clinical significance of reverse cholesterol transport Bleicher, J. M. and A. G. Lacko (1992), J Am Osteopath Assoc 92(5): 625-32. Abstract: Low levels of high-density lipoproteins have been consistently shown to be a major risk factor for coronary heart disease. However, the precise role of HDL in the prevention or reversal of atherosclerosis (or both) is unknown. It has been proposed that HDL functions jointly with the enzyme lecithin:cholesterol acyltransferase and the cholesteryl ester transfer protein to facilitate the movement of cholesterol from tissues to the liver. This mechanism--referred to as reverse cholesterol transport--has been shown to be an important physiologic mechanism. However, its clinical significance, though intriguing, is unclear. This article reviews recent advances concerning the components of reverse cholesterol transport and evaluates their potential significance in the early diagnosis and treatment of atherosclerosis. |
| Physiologic testosterone levels in normal men suppress high-density lipoprotein cholesterol levels Bagatell, C. J., R. H. Knopp, et al. (1992), Ann Intern Med 116(12 Pt 1): 967-73. Abstract: OBJECTIVE: To investigate the role of physiologic levels of testosterone in the control of lipoproteins in healthy men. DESIGN: A double-blind, randomized study. SETTING: A university community. PARTICIPANTS: Fifteen healthy men, ages 20 to 36 years. INTERVENTION: We induced acute, reversible hypogonadism in five normal men by administering daily subcutaneous injections of the gonadotropin-releasing-hormone (GnRH) antagonist, Nal-Glu, for 6 weeks. Another group of five normal men received Nal-Glu plus weekly injections of testosterone enanthate, 100 mg/wk, thereby maintaining normal serum testosterone levels. Five additional men received placebo injections. MEASUREMENTS: Plasma lipids, including high-density lipoprotein (HDL) subfractions HDL2 and HDL3, apoprotein A1, and serum levels of gonadotropins, estradiol, and testosterone were measured before, during, and after treatment. RESULTS: At the end of the treatment period, HDL cholesterol levels in men receiving Nal-Glu increased by 26% (95% CI, 18% to 34%; P less than 0.05). Levels of HDL2, HDL3, and apoprotein A1 increased by 63% (CI, 16% to 110%), 17% (CI, 3% to 31%), and 17% (CI, 5% to 29%), respectively (P less than 0.05 for each parameter). Total cholesterol increased by 12% (CI, 2% to 22%). Low-density lipoprotein (LDL) cholesterol and triglyceride concentrations did not change. No statistically significant changes occurred in any lipid measurement in men receiving Nal-Glu plus androgen replacement or placebo (P greater than 0.05). CONCLUSIONS: Experimental hypogonadism induced by administration of a GnRH antagonist results in a statistically significant increase in HDL cholesterol, including HDL2 and HDL3. These effects are most likely due to decreased androgen levels because they are reversed by administration of antagonist together with testosterone. Our results imply that androgen levels in the normal adult male range have a suppressive effect on HDL cholesterol concentration and may contribute to the increased risk for coronary artery disease in men. |
| Physiological concentration of 17beta-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury: role of NO Hayashi, T., M. Jayachandran, et al. (2000), Arterioscler Thromb Vasc Biol 20(6): 1613-21. Abstract: The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17beta-estradiol (E(2)) on high cholesterol diet- (HCD; standard diet and 1% cholesterol) and balloon injury-induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E(2) (100 microg x kg(-1) x d(-1)); Group 3, HCD; Group 4, HCD plus a moderate dose of E(2); Group 5, HCD plus a low dose of E(2) (20 microg x kg(-1) x d(-1)); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E(2) was increased up to 282.2+/-45.5 pg/mL in Group 2, 263.0+/-41.5 pg/mL in Group 4, 87. 9+/-18.8 pg/mL in Group 5, and 45.6+/-7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E(2) treatment, whereas E(2) decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E(2) restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E(2) increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E(2) concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E(2) can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E(2). |
| Physiological levels of estradiol stimulate plasma high density lipoprotein2 cholesterol levels in normal men Bagatell, C. J., R. H. Knopp, et al. (1994), J Clin Endocrinol Metab 78(4): 855-61. Abstract: Premenopausal women have a lower risk of coronary artery disease than men or postmenopausal women; estrogens are thought to contribute to this lower risk. Administration of exogenous estrogen to post-menopausal women increases plasma high density lipoprotein (HDL) cholesterol and may reduce mortality from coronary disease in users. Although many investigations have examined the roles of estrogen in the regulation of lipoproteins in women, little attention has been directed to estrogen regulation of lipids in men. We designed a paradigm to study the role of physiological levels of estradiol (E2) on plasma lipoproteins in healthy men. We used a GnRH antagonist, Nal-Glu, to suppress endogenous steroid hormones in healthy men. We then administered testosterone (T) enanthate (100 mg, im, weekly) to restore T levels to the baseline range, and we administered an aromatase inhibitor, testolactone (Teslac), to prevent the normal conversion of T to E2, thereby producing a selective estrogen deficiency state in normal young men. As controls, we administered Nal-Glu and T along with placebo Teslac to a separate group of men; a third group of men received all placebo medications. We found that in men who received Nal-Glu plus T plus Teslac, E2 levels were profoundly suppressed during treatment, whereas T levels remained in the baseline range. Plasma HDL cholesterol, particularly, the HDL2 fraction, decreased significantly in response to the low serum E2 level. Plasma apoprotein-AI levels also decreased significantly. Plasma LDL and triglyceride levels did not change. All hormone and lipoprotein parameters returned to baseline within 4 weeks after treatment ended. In men who received Nal-Glu plus T, plasma HDL and apoprotein-AI decreased, but these decreases did not achieve statistical significance. Only a small decrease in HDL2 cholesterol was seen in these men. There were no hormonal or lipid changes in the placebo group. We conclude that in men, physiological levels of E2 are important in maintaining plasma levels of HDL cholesterol, especially the HDL2 fraction. These observations suggest that estrogen, in the amount normally produced in men, may offer some degree of protection against cardiovascular disease in males, as they do in women. |
| Physiological mechanisms for the seasonal changes in serum cholesterol level Donahoo, W. T. and R. H. Eckel (2004), Arch Intern Med 164(22): 2506; author reply 2506-7. |
| Physiological responses to increased dietary cholesterol: the case of the egg man Jones, M. P. and D. M. Heuman (1991), Hepatology 14(6): 1291-3. |
| Physiopathology of cholesterol biliary calculi Mendez-Sanchez, N. and L. Uscanga (1991), Rev Gastroenterol Mex 56(3): 137-43. Abstract: The development of gallstones into the gallbladder is a dynamic event that comprises many contributing factors. In this work we reviewed the main factors such as physico-chemical properties of the major components of bile, with the purpose of obtain better understanding of the pathogenesis of cholesterol gallstones. |
| Phytoestrogen alpha-zearalanol inhibits atherogenesis and improves lipid profile in ovariectomized cholesterol-fed rabbits Dai, S., J. Duan, et al. (2004), Endocrine 25(2): 121-9. Abstract: Although favorable effects of estrogen replacement therapy on atherosclerosis have been recognized, the benefit versus risk of estrogen replacement on overall cardio- vascular health remains controversial. The main adverse effect jeopardizing the clinical usage of estrogen is the increased risk of breast and endometrial cancer. Zearalenone (ZEN) is a universal endogenous hormone possessing estrogen-like effects and facilitating plant growth. alpha-Zearalanol (alpha-ZAL), a new phytoestrogen, is a reductive product of ZEN. Our preliminary evidence suggested that alpha-ZAL is anti-atherosclerotic. The aim of this study was to examine the effect of alpha-ZAL on atherosclerotic formation and serum lipid profile. Adult female nulliparous rabbits were ovariectomized or sham-operated and fed a high-cholesterol diet with different doses of alpha-ZAL or 17beta-estradiol for 12 wk. The aortic intimal atherosclerotic plaque was significantly larger in the cholesterol-fed group compared to control and sham groups. alpha-ZAL and 17beta-estradiol treatments significantly reduced plaque formation and improved serum profile of lipid (TC, TG, HDL-C, and LDL-C) and lipoprotein (ApoAl and ApoB). Both alpha-ZAL and 17beta-estradiol reconciled ovariectomy-induced uterine atrophy, although alpha-ZAL was significantly less potent than 17beta-estradiol in stimulating uterine growth. Our findings indicate that the phytoestrogen alpha-ZAL has an important anti-atherogenic property, analogous to that of estrogen. |
| Phytosterols and cholesterol metabolism Ostlund, R. E., Jr. (2004), Curr Opin Lipidol 15(1): 37-41. Abstract: PURPOSE OF REVIEW: Phytosterols are plant sterols structurally similar to cholesterol that act in the intestine to lower cholesterol absorption. Because they have very low systemic absorption and are already present in healthy diets, increasing the intake of phytosterols may be a practical way to reduce coronary heart disease with minimum risk. RECENT FINDINGS: Phytosterols displace cholesterol from intestinal micelles, reducing the pool of absorbable cholesterol, but they are also rapidly taken up by enterocytes and increase expression of the adenosine triphosphate-binding cassette A1 sterol transporter. Phytosterol esters dissolved in food fat reduce LDL-cholesterol by 10% at a maximum effective dose of 2 g/day. However, this work probably understates the true effectiveness of phytosterols because it does not account for those naturally present in baseline diets. Single meal studies show that phytosterols in intact foods are bioactive at doses as low as 150 mg. The potential effectiveness of phytosterols has been improved in several ways. Individuals most likely to respond have been identified as having high cholesterol absorption and low cholesterol biosynthesis. Phytosterols can be emulsified with lecithin and delivered in non-fat or low-fat foods and beverages, and the amount of fat in fat-based preparations can be reduced substantially with the retention of bioactivity. SUMMARY: Phytosterols effectively reduce LDL-cholesterol when given as supplements, and the smaller amounts in natural foods also appear to be important. Future work will focus on the better delivery of phytosterols in natural foods and supplements and on further defining the mechanisms of action. |
| Phytosterols and lecithin do not have an additive effect in lowering plasma and hepatic cholesterol levels in diet-induced hypercholesterolemic rats Shin, J., Y. J. Kim, et al. (2004), Biofactors 22(1-4): 173-5. Abstract: Both plant sterols and lecithin are used as dietary supplements for lowering blood cholesterol in Western countries. This study evaluated the possibility of an additive effect of these ingredients on the regulation of lipid concentrations and cholesterol metabolism. Male Sprague-Dawley rats were randomly divided into three groups, and fed one of the following diets for 5 weeks; high cholesterol diet (HCD), phytosterol mixture-supplemented diet (PD, HCD+0.25% phytosterols), or phytosterol mixture and lecithin-supplemented diet (PLD, PD+0.15% lecithin). Feeding the PD for 5 weeks resulted in a 34% and 41% decrease in plasma total- and VLDL+LDL-cholesterol levels, respectively, and a 23% decrease in hepatic cholesterol content compared to those for the HCD rats (p < 0.05). These cholesterol-lowering properties of the phytosterol mixture were also associated with the down-regulation of hepatic acyl CoA:cholesterol acytransferase (ACAT) activity (p < 0.05). Addition of lecithin plus phytosterol mixture to the hypercholesterolemic diet did not significantly affect blood and hepatic lipid concentrations (with the exception of 36% decrease in hepatic triglyceride level, p < 0.05) as well as hepatic ACAT activity compared to feeding the hypercholesterolemic diet supplemented with phytosterol alone. These results indicate that combining lecithin, at a 0.15% level, with a phytosterol mixture-supplemented diet does not exhibit an additive effect in regulating hepatic ACAT activity or lowering blood cholesterol in hypercholesterolemic rats. |
| Phytosterols partially explain differences in cholesterol metabolism caused by corn or olive oil feeding Howell, T. J., D. E. MacDougall, et al. (1998), J Lipid Res 39(4): 892-900. Abstract: To examine whether phytosterols in polyunsaturated oils account for their differential action on lipid metabolism compared with monounsaturated oils, 16 normolipidemic individuals consumed three 10-day experimental diets containing corn oil (high in polyunsaturated fatty acids and phytosterols), olive oil (high in monounsaturated fatty acids and low in phytosterols), or olive oil supplemented with phytosterols given at twice the level naturally found in corn oil (high in monounsaturated fatty acids and phytosterols). Plasma total cholesterol concentrations after both the olive oil and the olive oil-phytosterol treatments were higher (P < 0.001) than those after the corn oil treatment. Olive oil treatment resulted in greater (P < 0.05) plasma LDL-cholesterol and triglyceride concentrations compared to corn oil treatment. Addition of the phytosterol mixture to the olive oil diet resulted in suppression of the significant differences in LDL-cholesterol and triglyceride concentrations between corn and olive oil. Free cholesterol fractional synthetic rates determined by deuterium incorporation were lower (P < 0.05) with olive oil treatment compared to corn oil treatment; the significance of this difference was abolished with the addition of phytosterols to the olive oil diet. These results suggest that phytosterols are partly responsible for the differences in plasma cholesterol levels and synthesis observed between polyunsaturated and monounsaturated oils. |
| Phytosterols that are naturally present in commercial corn oil significantly reduce cholesterol absorption in humans Ostlund, R. E., Jr., S. B. Racette, et al. (2002), Am J Clin Nutr 75(6): 1000-4. Abstract: BACKGROUND: Although supplementing the diet with large quantities of phytosterols reduces cholesterol absorption and LDL-cholesterol concentrations, very little is known about the smaller amounts of phytosterols present naturally in food. Vegetable oils are the richest dietary source of phytosterols; corn oil contains 0.77% phytosterols by weight. OBJECTIVE: We tested the hypothesis that removing phytosterols from corn oil would increase cholesterol absorption when measured in single-meal tests containing corn oil as a source of fat. DESIGN: Free and esterified phytosterols were removed from corn oil on a kilogram scale by a new technique of competitive saturation adsorption to silica. Healthy subjects with a mean (+/-SEM) serum cholesterol concentration of 5.10 +/- 0.18 mmol/L received an otherwise sterol-free test breakfast on 2 occasions 2 wk apart that contained 35 mg hexadeuterated cholesterol and 30-35 g of a corn oil preparation. The plasma enrichment of tracer was measured by negative ion mass spectrometry. RESULTS: Cholesterol absorption was 38.0 +/- 10.2% higher after consumption of the sterol-free corn oil than after consumption of commercial corn oil with an identical fatty acid content (P = 0.005; n = 10). When corn oil phytosterols were added back to sterol-free corn oil at a concentration of 150 mg/test meal, cholesterol absorption was reduced by 12.1 +/- 3.7% (P = 0.03; n = 5) and by 27.9 +/- 9.1% (P = 0.01; n = 10) after inclusion of 300 mg phytosterols. CONCLUSIONS: Phytosterols comprising < 1% of commercial corn oil substantially reduced cholesterol absorption and may account for part of the cholesterol-lowering activity of corn oil previously attributed solely to unsaturated fatty acids. |
| Pigment interferes with cholesterol analysis in erythrocyte lipid extracts: a procedure for removal Wang, W. Q. and A. Gustafson (1994), Acta Chem Scand 48(8): 699-700. Abstract: Removal of pigments from erythrocyte lipid extracts was achieved simply by adding isopropyl alcohol (2 ml) and silica gel H (0.05 g) to an aliquot of dried extract. This procedure is superior to other available methods because of its simplicity and high efficiency. |