| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effect and cellular site of action of cysteine protease inhibitors on the cholesterol esterification pathway in macrophages and Chinese hamster ovary cells Schissel, S. L., N. Beatini, et al. (1995), Biochemistry 34(33): 10463-73. Abstract: Stimulation of intracellular cholesterol esterification, which is catalyzed by the enzyme acyl-CoA:cholesterol O-acyltransferase (ACAT), by atherogenic lipoproteins in macrophages is a key step in the development of atheroma foam cells. Since other aspects of intracellular cholesterol metabolism involve proteolytic reactions, we looked for evidence of intracellular proteolysis in the stimulation of the cholesterol esterification pathway. When macrophages and CHO cells were incubated with the cysteine protease inhibitor N-acetylleucylleucylnorleucinal (ALLN), the ability of beta-very-low-density lipoprotein (beta-VLDL) and free cholesterol-rich liposomes to stimulate cholesterol esterification was inhibited by 60-90%. Epoxysuccinylleucylamido-3-methylbutane ethyl ester (EST), a cysteine protease inhibitor structurally different from ALLN, also inhibited beta-VLDL-induced cholesterol esterification in CHO cells. The inhibitory effect of the protease inhibitors could not be explained by decreased net expansion of cellular cholesterol pools, inhibition of lipoprotein cholesteryl ester hydrolysis, or blockage of cholesterol trafficking through the lysosomal pathway. Furthermore, stimulation of cholesterol esterification by 25-hydroxycholesterol and sphingomyelinase was not inhibited by ALLN, indicating that ALLN is not acting as a direct ACAT inhibitor in the cells, and suggesting that the ALLN effect is specific for methods of stimulating cholesterol esterification that expand cellular cholesterol pools. Previous studies have shown that inhibition of protein synthesis (e.g., by cycloheximide) stimulates cholesterol esterification in macrophages and CHO cells, suggesting the presence of a short-lived protein inhibitor of cholesterol esterification. Herein, we show that, when added after cycloheximide, ALLN does not inhibit cycloheximide-induced cholesterol esterification in either cell type. The data in this report are consistent with a novel model in which a proteolytic reaction mediates the stimulation of cholesterol esterification specifically by expanded cellular cholesterol pools. The apparent protease-dependent step is not dependent upon lysosomal trafficking of cholesterol and is proximal to the ACAT enzyme itself; it may function by cleaving an endogenous inhibitor of the interaction of expanded cellular cholesterol pools with ACAT. |
| Effect of 17 alpha-dihydroequilin sulfate, a conjugated equine estrogen, and ethynylestradiol on atherosclerosis in cholesterol-fed rabbits Sulistiyani, S. J. Adelman, et al. (1995), Arterioscler Thromb Vasc Biol 15(7): 837-46. Abstract: The effect of 17 alpha-dihydroequilin sulfate (DHES), a water-soluble estrogen of conjugated estrogens (Premarin), and ethynylestradiol (EE), a commonly used estrogen found in many oral contraceptives, on the development of atherosclerosis was studied in rabbits fed an atherogenic diet (0.2% cholesterol) for 24 weeks. Ten animals were given 15 micrograms. kg-1.d-1 EE, 10 received 3.8 mg.kg-1.d-1 of DHES, and the remaining 10 sham-ovariectomized and 10 ovariectomized animals served as cholesterol-fed controls. These doses were chosen to have similar estrogenic potency. Plasma cholesterol concentrations increased to about 900 mg/dL and did not differ among the experimental groups. After 24 weeks, plasma beta-VLDL and HDL cholesterol concentrations were the same for all cholesterol-fed groups, while LDL cholesterol was significantly higher in the two estrogen-treated groups. In spite of this, both EE and DHES significantly reduced atherosclerosis by 35% in the aortic arch and 75% to 80% in the thoracic and abdominal aorta. The reduction in atherosclerosis was seen in animals with a wide range (400 to 1400 mg/dL) of plasma cholesterol concentrations and was independent of lipoprotein profile. beta-VLDL isolated from estrogen-treated animals was not significantly different from control beta-VLDL in its ability to stimulate cholesterol accumulation in THP-1 macrophages in culture. This suggests that the protective effect of estrogens on the development of atherosclerosis is not mediated by qualitative differences in beta-VLDL that affect uptake by macrophages. The results of this study extend our knowledge of the range of estrogens that reduce atherosclerosis. Given the lack of effect on plasma lipid and lipoprotein concentrations, these data are consistent with the conclusion that estrogens exert some of this beneficial effect directly at the level of the arterial wall by influencing certain key components in the pathogenesis of atherosclerosis. |
| Effect of 20 days' bed rest on the reverse cholesterol transport system in healthy young subjects Yanagibori, R., K. Kondo, et al. (1998), J Intern Med 243(4): 307-12. Abstract: OBJECTIVES: To study the effects of 20 days of bed rest on HDL cholesterol, lipoprotein lipase, hepatic triglyceride lipase, cholesterol ester transfer protein and lecithin-cholesterol acyltransferase. DESIGN: A 20-day intervention study. SETTING: Makita general hospital. SUBJECTS: Five male and five female healthy participants, mean age 20.4 years, range 19-24 years. INTERVENTIONS: Twenty days of bed rest. MAIN OUTCOME MEASURES: Lipid, lipoprotein, lipoprotein lipase, hepatic triglyceride lipase, cholesterol ester transfer protein and lecithin-cholesterol acyltransferase. RESULTS: Fasting HDL, HDL2 and HDL3 cholesterol levels decreased from 1.748 to 1.404 mmol L(-1) (P < 0.01), from 0.807 to 0.628 mmol L(-1) (P < 0.01) and from 0.939 to 0.784 mmol L(-1) (P < 0.05), respectively, while VLDL triglyceride levels increased from 0.365 to 0.754 mmol L(-1) (P < 0.05). Plasma post-heparin lipoprotein lipase activity decreased from 0.494 to 0.418 micromol mL(-1) h(-1) (P < 0.01), but plasma post-heparin hepatic triglyceride lipase activity and cholesterol ester transfer protein activity did not change during bed rest. Lecithin-cholesterol acyltransferase activity increased from 72.5 to 84.8 nmol mL(-1) h(-1) (P < 0.001). CONCLUSIONS: Twenty days of bed rest induced a decline in HDL cholesterol levels and an increase in VLDL triglyceride levels. When considering lipoprotein lipase, hepatic triglyceride lipase, cholesterol ester transfer protein and lecithin-cholesterol acyltransferase as factors in the decreased HDL cholesterol, the contribution of lipoprotein lipase is suggested. |
| Effect of 25-hydroxycholesterol and progesterone on esterification of cholesterol, viscosity, and protein-lipid interactions in macrophage membranes Dushkin, M. I., N. G. Kolosova, et al. (2000), Biull Eksp Biol Med 129(2): 145-8. |
| Effect of 26-oxygenosterols from Ganoderma lucidum and their activity as cholesterol synthesis inhibitors Hajjaj, H., C. Mace, et al. (2005), Appl Environ Microbiol 71(7): 3653-8. Abstract: Ganoderma lucidum is a medicinal fungus belonging to the Polyporaceae family which has long been known in Japan as Reishi and has been used extensively in traditional Chinese medicine. We report the isolation and identification of the 26-oxygenosterols ganoderol A, ganoderol B, ganoderal A, and ganoderic acid Y and their biological effects on cholesterol synthesis in a human hepatic cell line in vitro. We also investigated the site of inhibition in the cholesterol synthesis pathway. We found that these oxygenated sterols from G. lucidum inhibited cholesterol biosynthesis via conversion of acetate or mevalonate as a precursor of cholesterol. By incorporation of 24,25-dihydro-24,25-3H2lanosterol and 3-3Hlathosterol in the presence of ganoderol A, we determined that the point of inhibition of cholesterol synthesis is between lanosterol and lathosterol. These results demonstrate that the lanosterol 14alpha-demethylase, which converts 24,25-dihydrolanosterol to cholesterol, can be inhibited by the 26-oxygenosterols from G. lucidum. These 26-oxygenosterols could lead to novel therapeutic agents that lower blood cholesterol. |
| Effect of 3,4-di(OH)-cinnamate synthetic derivative on plasma and hepatic cholesterol level and antioxidant enzyme activities in high cholesterol-fed rats Park, E. J., S. Lee, et al. (2004), J Biochem Mol Toxicol 18(5): 279-87. Abstract: The effect of 3,4-di(OH)-phenylpropionic acid (L-phenylalanine methyl ester) amide (SL-1063), a synthetic derivative of 3,4-di(OH)-cinnamate, on the cholesterol metabolism and antioxidant enzyme system was examined in rats. Diets that included either SL-1063 (0.046%, w/w) or lovastatin (0.02%, w/w) as a supplement, plus 1 g cholesterol/100 g diet were fed to rats ad libitum for 5 weeks. The total plasma cholesterol and triglyceride levels were significantly lowered by the SL-1063 supplement compared to the control group. Meanwhile, the levels of plasma HDL-cholesterol and ratio of HDL-cholesterol/total cholesterol (%) were significantly higher in the SL-1063 group than in the control group. However, the lovastatin supplement did not affect the plasma lipid level. The hepatic cholesterol level and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity were significantly lowered in the lovastatin group compared to the SL-1063 group; however, the hepatic triglyceride level did not differ among the groups. The activity of hepatic acyl CoA: cholesterol acyltransferase (ACAT), the enzyme that catalyzes hepatic cholesterol esterification, was significantly lower in the lovastatin and SL-1063 groups than in the control group. Furthermore, the SL-1063 supplement elevated the excretion of fecal sterols. As regards the hepatic antioxidant enzyme system, the superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) activities were all significantly higher in the SL-1063 group compared to the control group, whereas only the GR activity was significantly increased by the lovastatin supplement. No marked difference in the GSH levels and glucose-6-phosphate dehydrogenase (G6PD) activities was observed among the groups. The levels of plasma and hepatic thiobarbituric acid reactive substances (TBARS) were lowered by the SL-1063 supplement compared to the control group. Accordingly, the current results suggest that SL-1063, a synthetic derivative of 3,4-di(OH)-cinnamate, is effective in lowering the plasma lipids and improving the antioxidant enzyme system. |
| Effect of 347-serine mutation in apoprotein A-IV on plasma LDL cholesterol response to dietary fat Jansen, S., J. Lopez-Miranda, et al. (1997), Arterioscler Thromb Vasc Biol 17(8): 1532-8. Abstract: Lipid response to dietary fat and cholesterol is, to a large extent, genetically controlled. Apoprotein (apo) A-IV has been related to fat absorption and to the activation of some of the enzymes involved in lipid metabolism. One mutation has been described in the apo A-IV gene that causes substitution of Ser for Thr at position 347. To study the influence of this mutation on the plasma LDL cholesterol (LDL-C) response in diets of various fat content and fatty acid saturation, 41 healthy male subjects were studied, 25 of whom were homozygous for the Thr allele (347Thr) and the rest who were either homozygous (n = 2) or heterozygous carriers of the Ser allele (347Ser). They consumed three consecutive diets, each of 4 weeks' duration: one rich in saturated fat (SFA diet: 38% fat, 20% saturated), a National Cholesterol Education Program (NCEP) type 1 diet (28% fat, 10% saturated), and a third rich in monounsaturated fat (MUFA diet; 38% fat, 22% monounsaturated). Carriers of the 347Ser allele presented a greater decrease in total cholesterol (-0.7 vs -0.44 mmol/L, P <.034), LDL-C (-0.62 vs -0.31 mmol/L, P <.012), and apo B (-14 vs -8 mg/dL, P <.01) levels when they were switched from the SFA to the NCEP type 1 diet than homozygous carriers of the 347Thr allele. The change from the NCEP type 1 to the MUFA diet resulted in a greater increase in total cholesterol (0.18 vs -0.05 mmol/L, P <.028) and apo B (5 vs -1 mg/dL, P <.006) levels in the 347Ser than in the 347Thr individuals. In a previous study, we demonstrated that the G-->A polymorphism at position -76 of the gene promoter of apo A-I affects the LDL-C response to dietary fat. We therefore decided to study the effect of the interaction between these mutations on this response. We found that both mutations have an additive effect on total cholesterol, LDL-C, and apo B dietary-induced changes. Our results suggest that total cholesterol and LDL-C response to dietary fat is influenced by the 347Ser mutation of apo A-IV. |
| Effect of 360His mutation in apolipoprotein A-IV on plasma HDL-cholesterol response to dietary fat Jansen, S., J. Lopez-Miranda, et al. (1997), J Lipid Res 38(10): 1995-2002. Abstract: In order to determine whether genetic variability of apolipoprotein (apo) A-IV is responsible for the improvement in lipid profile when dietary saturated fats are replaced by carbohydrates or monounsaturated fats, 41 healthy male subjects were studied: 33 were homozygous for the 360Gln allele and 8 were heterozygote carriers of the 360His allele. These were administered three consecutive 4-week diets. The first was a diet rich in saturated fat (SAT diet, with 38% fat, 20% saturated. This was followed by a low fat diet (NCEP-I, with < 30% fat, < 10% saturated). The final diet was rich in monounsaturated fat (MUFA diet, with 38% fat, 22% monounsaturated). There was no difference in plasma lipid and apolipoprotein levels of both groups of individuals after consuming the SAT diet. Switching from this diet to the NCEP-I diet, carriers of the 360His allele presented a greater decrease in high density lipoprotein-cholesterol (HDL-C) (-10 vs. -1 mg/dL, P < 0.004) and apoA-I levels (-19 vs. -8 mg/dL, P < 0.037). Similarly, replacement of carbohydrates by monounsaturated fats produced a greater increase in HDL-C (9 vs. 1 mg/dL, P < 0.003) and apoA-I levels (9 vs. 2 mg/dL, P < 0.036) in carriers of the 360His mutation. Lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) activities and apoA-IV levels were also measured. However, no genotype-related differences were observed for these parameters. Our results suggest that variability in HDL-C and apoA-I response to diet is, at least partially, determined by the 360His mutation of apoA-IV. |
| Effect of 3-substituted Delta8(14)-15-ketosterols on cholesterol metabolism in hepatoma Hep G2 cells Kisseleva, A. F., L. E. Goryunova, et al. (1999), Biochemistry (Mosc) 64(4): 456-63. Abstract: The effects of 3-substituted Delta8(14)-15-ketosterols--3beta-(2-hydroxyethoxy)-, 3beta-(2-propenyloxy)-, 3beta-2(R,S),2,3-oxidopropyloxy-, 3beta-2(R,S),2,3-dihydroxypropyloxy-, 3beta-(2-oxoethoxy)-, 3beta-2(R,S),2-acetoxy-3-acetamidopropyloxy-, and 3beta-2(R,S), 2-hydroxy-3-acetamidopropyloxy-5alpha-cholest-8(14)-en-15-o nes--on cholesterol metabolism were studied in human hepatoma Hep G2 cells. 3beta-(2-Propenyloxy)-, 3beta-(2-oxoethoxy)-, and 3beta-2(R,S),2, 3-oxidopropyloxy-5alpha-cholest-8(14)-en-15-ones inhibited cholesterol biosynthesis without any effect on triglyceride biosynthesis, while 3beta-2(R,S),2-acetoxy-3-acetamidopropyloxy- and 3beta-2(R,S), 2-hydroxy-3-acetamidopropyloxy-5alpha-cholest-8(14)-en-15-o nes inhibited both cholesterol biosynthesis and triglyceride biosynthesis at concentrations exceeding 10 microM. 3beta-2(R,S),2, 3-Dihydroxypropyloxy-5alpha-cholest-8(14)-en-15-one, effectively inhibiting cholesterol biosynthesis, was found also to be toxic in Hep G2 cells at micromolar concentrations. 3beta-2(R,S),2, 3-Oxidopropyloxy-5alpha-cholest-8(14)-en-15-one effectively inhibited cholesterol acylation. All the tested compounds decreased the HMG-CoA reductase mRNA level at concentrations exceeding 10 microM; however, they did not affect the LDL receptor mRNA level. Among the compounds tested, only 3beta-hydroxy-5alpha-cholest-8(14)-en-15-one decreased the uptake and internalization of LDL-associated cholesteryl esters, being as effective as 25-hydroxycholesterol. |
| Effect of 4-cholesten-3-one on lecithin-cholesterol acyltransferase activity and the lipid concentration in the serum of normocholesterolaemic and hypercholesterolaemic rats Tallova, J., M. Dobiasova, et al. (1990), Physiol Bohemoslov 39(2): 119-23. Abstract: Male Wistar strain rats and PHHC (Prague hereditary hypercholesterolaemic) rats received an intraperitoneal injection of 4-cholesten-3-one for five days. Lecithin-cholesterol acyltransferase activity and total cholesterol, triglyceride and phospholipid levels were determined in their serum. A significant drop in the total cholesterol level was found in normocholesterolaemic Wistar rats after the administration of cholestenone. The serum triglyceride content remained unaltered and the phospholipid concentration showed a downward trend. Lecithin-cholesterol acyltransferase activity was also significantly reduced. In PHHC rats, no significant changes occurred in total cholesterol, triglyceride and phospholipid levels, or in lecithin-cholesterol acyltransferase activity, after the administration of 4-cholesten-3-one. A comparison of serum 4-cholesten-3-one concentrations in the two groups of experimental animals shows that the turnover time for this substance in hypercholesterolaemic rats is only half as long as in normocholesterolaemic rats. |
| Effect of 5H-alpha-cholest-8(14)-en-3-beta-ol-15-one on cholesterol metabolism in cultured rabbit hepatocytes Mambetisaeva, E. T., V. A. Kosykh, et al. (1993), Biokhimiia 58(2): 261-7. Abstract: The effects of 15-ketosterol on cholesterol metabolism in cultured rabbit hepatocytes were characterized by the following parameters: a) cholesterol synthesis, b) apo B and apo E secretion, c) bile acid synthesis. 15-Ketosterol used at therapeutic concentration (0.25 microM) reduced cholesterol synthesis (by 50%). Marked inhibition (by 70%) of apo B and apo E secretion was observed for this agent. Synthesis and secretion of the total 14C-labeled protein remaining unchanged. 15-Ketosterol did not influence the bile acid synthesis in primary culture of rabbit hepatocytes. These results are suggestive of a new putative mechanism of hyperlipidemic action of 15-ketosterol by a simultaneous decrease of hepatic cholesterol synthesis and secretion of apo B-containing particles. |
| Effect of a 10-day animal fat-free diet on cholesterol and glucose serum levels, blood pressure and body weight in 50-year-old volunteers Slavicek, J., O. Kittnar, et al. (2001), Sb Lek 102(4): 519-25. Abstract: The morbidity and mortality of cardiovascular diseases is high in developed countries including Czech Republic. The lifestyle decreases it in 50%. The aim of this work was to ascertain if the short lasting stay without stress and with vegetarian diet (without eggs) and physical activity is able to decrease the main risk factors of cardiovascular diseases. In 106 volunteers, mean age 49.1 (+/- 14.1) years, 83 women and 23 men, the body weight, blood pressure, serum cholesterol and blood glucose (Accutrend GC, Boehringer, Mannheim, BRD) have been measured before and after the stay at the same conditions. Eighty persons were healthy, seven persons with essential hypertension, eight persons with ischemic heart disease, four persons with diabetes mellitus and seven persons with other than cardiovascular diseases. In some persons the lipid spectrum was measured. Cholesterol decreased in blood serum from 4.9 to 4.3 mmol/l (11%--p < 0.01), blood glucose decreased from 4.2 to 3.3 mmol/l (p < 0.05), blood pressure systolic from 121.5 to 117.4 mm Hg (p < 0.01) and diastolic from 76.5 to 73.8 mm Hg (p < 0.05), body weight was not significantly changed. Our results showed, that 10-days lasting stay containing vegetarian diet and physical activity decreased the risk factors of cardiovascular diseases in 50 years-old volunteers. |
| Effect of a cholesterol synthesis inhibitor (BM 15.766) in the presence and absence of HDL on corticosteroidogenesis of isolated zona glomerulosa and fasciculata cells Toth, I. E., K. S. Szalay, et al. (1990), J Steroid Biochem Mol Biol 37(5): 687-91. Abstract: The effect of the cholesterol synthesis inhibitor BM 15.766, 4-2-1-(4-chlorocinamyl)piperazin-4-ylethyl-benzoic acid on the corticosteroid production was studied in order to reveal the importance of endogenous cholesterol synthesis in the function of zona glomerulosa and zona fasciculata cells of rats. Attempts were made to compensate the effect of BM 15.766 through the application of high-density lipoproteins (HDL). Electron microscopy was used to trace the binding and intracellular accumulation of colloidal gold-labelled HDL (HDL-Au, a cholesterol carrier), in the presence of the cholesterol biosynthesis inhibitor. The stimulation of both types of cells with ACTH was less effective in the presence of 2 x 10(-5) M BM 15.766. The inhibitory effect of BM 15.766 was most marked on the aldosterone production of the zona glomerulosa cells, and could not be reversed by addition of a small amount of HDL-Au. Corticosterone-aldosterone conversion was inhibited by 2 x 10(-5) M BM 15.766. ACTH-stimulated, short-term HDL uptake and internalization was not affected by the cholesterol synthesis inhibitor. The results suggest that certain metabolites of de novo cholesterol biosynthesis may participate in the control of aldosterone production. |
| Effect of a cholesterol-rich diet on the excitability of rabbit aorta Wong, K. K. (1996), Biochem Mol Biol Int 40(2): 389-93. Abstract: The level of plasma total cholesterol in rabbits after 8-week feeding on a cholesterol-rich diet was raised significantly. The excitability of the rabbit aorta in response to the depolarizing agent KCl was enhanced, demonstrating an increased sensitivity to KCl stimulation as well as an increase of the KCl-induced maximum tension. It is speculated that 7 weeks of hypercholesterol state may vary the membrane lipid composition, enhancing the aortic excitability in response to depolarizing agent. |
| Effect of a chronic therapy with the pineal hormone melatonin on cholesterol levels in idiopathic hypercholesterolemic patients Pittalis, S., P. Lissoni, et al. (1997), Recenti Prog Med 88(9): 401-2. |
| Effect of a coffee lipid (cafestol) on cholesterol metabolism in human skin fibroblasts Halvorsen, B., T. Ranheim, et al. (1998), J Lipid Res 39(4): 901-12. Abstract: Consumption of boiled coffee promotes an elevation of plasma cholesterol concentration in humans. The active compounds found in the lipid fraction of the coffee have been identified as the diterpenes cafestol and kahweol. We have studied the effects of pure cafestol on cholesterol metabolism in human skin fibroblasts (HSF). The uptake of 125I-labeled tyramine cellobiose-labeled low density lipoprotein (125ITC-LDL) was decreased by about 50% (P< 0.05) after 18 h preincubation time with cafestol (20 microg/ml), as compared to the control cells. The specific binding of radiolabeled LDL was reduced by 54% (P < 0.05) after preincubation for 18 h with cafestol. A reduced amount of LDL receptors was demonstrated by a protein-normalized Scatchard plot analysis (20% decrease in Bmax) as well as by immunoblotting (25%) after cafestol incubation. No significant effect was observed on the level of mRNA for the LDL receptor after 11 and 23 h incubation with cafestol. Furthermore, we transfected HSF cells with a promoter region for the LDL receptor gene linked to a reporter gene, chloramphenicol acetyl transferase (CAT). No change was seen in the CAT activity after incubation with cafestol (20 microg/ml). Moreover, cafestol caused a 2.3-fold (P < 0.05) higher incorporation of radiolabeled 14Coleic acid into cholesteryl esters after 24 h incubation, as compared to control cells, suggesting an increased acyl-CoA:cholesterol acyl transferase (ACAT) activity. Incorporation of 14Cacetate into cholesterol was reduced by approximately 40% (P < 0.05) with cafestol (20 microg/ml), as compared to control after 24 h preincubation, indicating a decreased 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity. Our results suggest that intake of cafestol may cause increased concentration of plasma cholesterol via the down-regulation of low density lipoprotein receptors by post-transcriptional mechanisms. |
| Effect of a community cholesterol screening program on serum total cholesterol level Hilton, T. C. and H. L. Kennedy (1991), Am J Cardiol 68(2): 247-9. |
| Effect of a diet based on low-fat foods enriched with nonesterified plant sterols and mineral nutrients on serum cholesterol Tikkanen, M. J., P. Hogstrom, et al. (2001), Am J Cardiol 88(10): 1157-62. Abstract: Plant sterols have been incorporated into nutritional fats to achieve cholesterol lowering, but studies using enrichment of low-fat foods with plant sterols have not been reported. Our study was aimed at determining the effect of dietary intake of low-fat foods containing natural nonesterified plant sterols together with recommended doses of calcium, magnesium, and potassium on serum cholesterol and low-density lipoprotein (LDL) cholesterol-lowering in persons with mild to moderate hypercholesterolemia. This was a randomized, double-blind, placebo-controlled feeding trial lasting 15 weeks and performed in 2 university hospital centers. Seventy-eight subjects aged 25 to 75 years with serum cholesterol concentrations varying between 6 mmol/L (232 mg/dl) and 8 mmol/L (310 mg/dl) were randomly allocated to active treatment consisting of intake of bread, meat products, and jam enriched with 1.25 to 5.0 g/day of plant sterols and the slightly elevated concentrations of mineral nutrients, or the corresponding placebo food items. Serum lipid, high-density lipoprotein cholesterol and calculated LDL cholesterol concentrations were determined. Seventy-one persons completed the trial. Reduction in serum total cholesterol was 8% in the active treatment group and 3% in the placebo group (p = 0.0071) and that of LDL cholesterol was 13% in the active treatment group and 5% in the placebo group (p = 0.0070). In conclusion, natural nonesterified plant sterols contained in low-fat food items and ingested in moderate doses reduced serum total and LDL cholesterol concentrations to the same extent as reported previously for esterified plant sterol derivatives added to nutritional fats. The presence of mineral nutrients in doses recommended for blood pressure-lowering did not interfere with the cholesterol-lowering efficacy of the sterols, providing a promising approach to dietary prevention of cardiovascular diseases. |
| Effect of a diet high in monounsaturated fat from almonds on plasma cholesterol and lipoproteins Spiller, G. A., D. J. Jenkins, et al. (1992), J Am Coll Nutr 11(2): 126-30. Abstract: The effect of almonds as part of a low saturated fat, low cholesterol, high-fiber diet was studied in 26 adults (13 men, 13 women). The baseline diet was modified in a similar way for all subjects by limiting meat, fatty fish, high-fat milk products, eggs, and saturated fat. Grains, beans, vegetables, fruit, and low-fat milk products were the foundation of the diet. During the almond diet period, raw almonds (100 mg/day) supplied 34 g/day of monounsaturated fatty acid (MUFA), 12 g/day of polyunsaturated fatty acid, and 6 g/day of saturated fatty acid. Almond oil was the only oil allowed for food preparation. There was a rapid and sustained reduction in low-density lipoprotein cholesterol without changes in high-density lipoprotein cholesterol. This was reflected in a total plasma cholesterol decrease from (means +/- SEM) 235 +/- 5.0 at baseline to 215 +/- 5.0 at 3 weeks, and to 214 +/- 5.0 mg/dl at 9 weeks (p less than 0.001). When the consumption of nuts high in MUFA increases the fat content of the diet, reduction rather than elevation of plasma cholesterol has to be expected, possibly due to the MUFA content of these nuts. |
| Effect of a dietary supplement combination on weight management, adipose tissue, cholesterol and triglycerides in obese subjects Gonzalez, M. J., J. R. Miranda-Massari, et al. (2004), P R Health Sci J 23(2): 121-4. Abstract: A combination dietary supplement containing vitamins, minerals, herbs, fibers and amino acids was studied to determine its safety and efficacy on weight/ fat loss, cholesterol and triglycerides in a double-blind, placebo-controlled trail. Total body weight, body fat %, waist and hip measurements, total cholesterol and triglycerides were evaluated before and after 6 weeks treatment with combination supplement or placebo. The study population consisted in 27 mildly to moderately obese, otherwise healthy, volunteers. After 6 weeks of treatment, the combination supplement had a statistically significant (p<0.001, mu=0.05) positive weight reducing effect (-8.59Lb vs. +2.14 Lb). This weight reduction was associated with a corresponding statistically significant (p<0.001, mu=0.05) decrease in body fat % in the treatment group (-2.88%) vs. the placebo (+0.86%). In addition, significant decreases in total cholesterol (-22.94 mg/dL) and triglycerides (-39.29 mg/dL) were obtained plus reductions in waist and hip measurements. These positive results lead us to conclude, that the combination supplement studied herein is a safe and effective way to assist in weight/fat reduction and decreases in total cholesterol and triglycerides in relatively short time (6 weeks). |