| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Effect of oxysterol treatment on cholesterol biosynthesis and reactive astrocyte proliferation in injured rat brain cortex Bochelen, D., M. Mersel, et al. (1995), J Neurochem 65(5): 2194-200. Abstract: We have reported previously that oxysterols inhibit astrogliosis and intracranial glioblastoma growth. To elucidate the mechanism of action of these molecules in vivo, we have investigated their effect on the cholesterol biosynthesis in the injured brain. In a bilateral lesion model, injection of liposomes containing 7 beta-hydroxy-cholesterol decreased 3Hacetate incorporation into neutral lipids and cholesterol by 30% and 40%, respectively. Structural analogues were tested using a unilateral lesion model. The injury did not significantly affect cholesterogenesis; injection of 7 beta-hydroxycholesterol or 7 beta-hydroxycholesteryl-3-oleate reduced acetate incorporation into cholesterol by 47% and 43%, respectively. Both 7-ketocholesteryl-3-oleate and 7 alpha-hydroxycholesteryl-3-oleate inhibited cholesterogenesis by 32%. As cholesterol and by-products of the cholesterol pathway play a key role in cell division, we have assessed the effect of oxysterols on reactive astrocyte proliferation. The incorporation of bromodeoxyuridine showed that up to 46% of astrocytes were proliferating 24 h after the injury. Injection of 12 nmol of 7 beta-hydroxycholesterol or 7 beta-hydroxycholesteryl-3-oleate reduced the labelling index to 26%, whereas the labelling index in the 7-keto-cholesteryl-3-oleate-treated cortex was 37%. These findings demonstrate that oxysterols are potent inhibitors of the endogenous cholesterol biosynthesis in brain and show a correlation between cholesterogenesis and reactive astrocyte proliferation. |
| Effect of oyster mushroom (Pleurotus Ostreatus) and its ethanolic extract in diet on absorption and turnover of cholesterol in hypercholesterolemic rat Bobek, P., L. Ozdin, et al. (1996), Nahrung 40(4): 222-4. Abstract: The effect of the diet containing 5% of powdered oyster mushroom (Pleurotus ostreatus) or an equivalent amount of mushroom ethanolic extract on cholesterol content in serum and liver, on its distribution in lipoproteins, absorption and turnover was studied in male Wistar rats (initial body weight about 70 g) fed a diet with 0.3% cholesterol. 12 weeks of feeding with whole oyster mushroom or mushroom extract reduced cholesterol level in serum by 52 and 33%, respectively. However, cholesterol content in liver was reduced only by whole oyster mushroom (by 20%). Diminished serum cholesterol level was mediated in 60% by reduction of cholesterol in very-low-density lipoproteins. Both whole oyster mushroom and mushroom extract increased the concentration of cholesterol in high-density lipoproteins. Consuming whole oyster mushroom decreased cholesterol absorption (estimated by dual-isotope plasma ratio method) by nearly 16% while no significant effect of mushroom extract could be demonstrated. Feeding the diet containing whole oyster mushroom or its extract reduced the half-times of decay curve of cholesterol-4-14C by 29 and 35%, respectively and reciprocally increased the fractional catabolic rate of plasma cholesterol. |
| Effect of pancreas transplantation on lipoprotein lipase, postprandial lipemia, and HDL cholesterol Foger, B., A. Konigsrainer, et al. (1994), Transplantation 58(8): 899-904. Abstract: Pancreas transplantation with systemic venous drainage of the graft causes elevated plasma levels of insulin, known to be a potent regulator of plasma lipoprotein metabolism. We studied 11 post-type I diabetic pancreas-kidney transplant recipients, 9 type I diabetic kidney transplant recipients displaying peripheral hyperinsulinemia due to subcutaneous insulin treatment, 11 nondiabetic kidney transplant recipients as controls for the effects of immunosuppressive medication, and 11 healthy control subjects, all matched for age, sex, and body mass index. We determined fasting lipids, lipoproteins and lipolytic enzymes, as well as postprandial lipid metabolism after a standardized oral fat load. High-density lipoprotein (HDL) cholesterol averaged 1.98 (0.40) mmol/L in pancreas-kidney transplant patients, clearly higher than that of kidney transplant recipients (1.52 (0.36) mmol/L, P < 0.05) or of controls (1.50 (0.38) mmol/L, P < 0.05). In pancreas-kidney transplant patients postprandial lipemia was lowest and lipoprotein lipase activity was highest (average 32% and 154%, respectively, of the mean of the controls) compared with nondiabetic kidney transplant recipients (P < 0.005, P < 0.05) and healthy controls (P < 0.001, P < 0.01). In type I diabetic kidney transplant recipients the levels of HDL cholesterol (1.88 (0.63) mmol/L), postprandial lipemia, and lipoprotein lipase activity were intermediate between pancreas-kidney transplant patients and healthy controls. The distinctly elevated HDL cholesterol in pancreas-kidney transplant patients can be readily explained by the low postprandial triglyceride levels resulting from a high activity of lipoprotein lipase. The very favorable lipid profile in post-diabetic pancreas-kidney transplant recipients could be expected to counteract the severe atherosclerotic risk of long-standing diabetes. |
| Effect of partially hydrolyzed guar gum (PHGG) on the bioaccessibility of fat and cholesterol Minekus, M., M. Jelier, et al. (2005), Biosci Biotechnol Biochem 69(5): 932-8. Abstract: The addition of a compound that lowers the intestinal uptake of fat and cholesterol might be an interesting strategy to reduce the risk of vascular disease. Partially hydrolyzed guar gum (PHGG) has been shown to have this effect in healthy volunteers after intake of a yogurt drink with 3 to 6% PHGG. In the present study a yogurt drink with 3% sunflower oil and 4% egg yolk was tested with 3% and 6% PHGG, and compared to a control without PHGG. Experiments were performed in a multi-compartmental model of the gastrointestinal tract, equipped to study the digestion and availability for absorption (bioaccessibility) of lipids. The results show that PHGG decreases the bioaccessibility of both fat and cholesterol in a dose-dependent manner. The bioaccessibility of fat was 79.4+/-1.7%, 70.8+/-2.5% and 60.1+/-1.1% for the control experiments and the experiments with 3% and 6% PHGG respectively. The bioaccessibility of cholesterol was 82.2+/-2.0%, 75.4+/-1.2% and 64.0+/-4.3% for the control and the experiments with 3% and 6% PHGG respectively. Additional experiments indicated that PHGG reduces bioaccessibility through the depletion flocculation mechanism. Depletion flocculation antagonizes the emulsification by bile salts and thus decreases lipolytic activity, resulting in a lower bioaccessibility of fat and cholesterol. Depletion flocculation with polymers might be an interesting mechanism, not described before, to reduce fat and cholesterol absorption. |
| Effect of peanut oil and randomized peanut oil on cholesterol and oleic acid absorption, transport, and distribution in the lymph of the rat Satchithanandam, S., T. J. Flynn, et al. (1999), Lipids 34(12): 1305-11. Abstract: Peanut oil was shown to be atherogenic in cholesterol-fed rats, rabbits, and monkeys. However, after randomization, a process in which the fatty acids in peanut oil are randomly rearranged, its atherogenicity was significantly reduced in cholesterol-fed rabbits and monkeys. The mechanism for this effect remains unknown. This study was designed to investigate whether the absorption, transport and distribution of dietary cholesterol and oleic acid in the lymph were altered in the presence of peanut oil or randomized peanut oil. Previous investigators collected lymph through the mesenteric duct for 6 h and analyzed lymph for cholesterol. In the present study, lymph fluids were collected at timed intervals for up to 8 h and then at 24 h via the thoracic duct. Cholesterol and oleic acid (fatty acid) were estimated not only in the whole lymph but also in lymph lipoprotein fractions and in major lipid fractions. A 24-h lymph collection will enhance accuracy as short-term fluctuations in lipid absorption will not affect the results. Thoracic duct lymph collection is quantitative compared to mesenteric duct lymph collection, which provides only a fraction of the total lymph. Rats were given a lipid emulsion containing either peanut oil or randomized peanut oil. The emulsion also contained cholesterol, oleic acid, and sodium taurocholate in saline and was given through a duodenal catheter. Results show that absorption, transport, and distribution of cholesterol and oleic acid in the lymph fluids were similar in both dietary groups. These results suggest that the atherogenicity of peanut oil may be due to other events taking place subsequent to the release of cholesterol-containing chylomicrons and very low density lipoprotein by the small intestinal epithelial cells into the blood or may be due to the triglyceride structure itself. |
| Effect of perindopril on the development of atherosclerosis in the cholesterol-fed rabbit Campbell, J. H., P. Fennessy, et al. (1992), Clin Exp Pharmacol Physiol Suppl 19: 13-7. Abstract: 1. The aim of the study was to examine the effect of the angiotensin-converting enzyme inhibitor perindopril on the development of atheroma in the cholesterol-fed rabbit. 2. The normal human carotid artery, like most large human arteries, has a preformed diffuse intimal thickening. To model this thickening, the right carotid artery of the 12-week-old rabbit had an expanded balloon catheter passed down it to remove the endothelium and partially damage the media. 3. Fourteen weeks after this operation, a myointimal thickening similar in almost all respects to the human intimal thickening had developed. The rabbits were then divided into six groups of six rabbits fed on: (i) a 1% cholesterol diet; (ii) a 1% cholesterol diet plus a hypotensive dose of perindopril (0.3 mg/kg per day); (iii) a 1% cholesterol diet plus a non-hypotensive dose of perindopril (0.01 mg/kg per day); (iv) a normal diet; (v) a normal diet plus a hypotensive dose of perindopril (0.3 mg/kg per day); and (vi) a normal diet plus a non-hypotensive dose of perindopril (0.01 mg/kg per day). 4. After 6 weeks of treatment the animals were sacrificed. There were ameliorating effects of both hypotensive and non-hypotensive doses of perindopril on the development of plaques, as determined by the area of intima covered by Oil Red-O-staining plaque and light microscopy. 5. Cell culture studies indicated that perindopril has no effect on smooth muscle proliferation, but increases collagen and non-collagen synthesis by smooth muscle cells and decreases their binding of the atherogenic lipoprotein beta-very low density lipoprotein (beta-VLDL).(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effect of peroxisome proliferators on Leydig cell peripheral-type benzodiazepine receptor gene expression, hormone-stimulated cholesterol transport, and steroidogenesis: role of the peroxisome proliferator-activator receptor alpha Gazouli, M., Z. X. Yao, et al. (2002), Endocrinology 143(7): 2571-83. Abstract: In this study, we hypothesized that many of the reported effects of phthalate esters and other peroxisome proliferators (PPs) in the testis are mediated by members of the PP- activated receptor (PPAR) family of transcription factors through alterations in proteins involved in steroidogenesis. Exposure of Leydig cells to PPs prevented cholesterol transport into the mitochondria after hormonal stimulation and inhibited steroid synthesis, without altering total cell protein synthesis or mitochondrial and DNA integrity. PPs also reduced the levels of the cholesterol-binding protein peripheral-type benzodiazepine receptor (PBR) because of a direct transcriptional inhibition of PBR gene expression in MA-10 Leydig cells. MA-10 cells contain mRNAs for PPARalpha and PPARbeta/delta, but not for PPARgamma. In vivo treatment of mice with PPs resulted in the reduction of both testis PBR mRNA and circulating testosterone levels, in agreement with the proposed role of PBR in steroidogenesis. By contrast, liver PBR mRNA levels were increased, in agreement with the proposed role of PBR in cell growth/tumor formation in nonsteroidogenic tissues. However, PPs did not inhibit testosterone production and testis PBR expression in PPARalpha-null mice. These results suggest that the antiandrogenic effect of PPs is mediated by a PPARalpha-dependent inhibition of Leydig cell PBR gene expression. |
| Effect of pesticides carbaryl and phorate on serum cholesterol level in fish, Clarias batrachus (Linn) Jyothi, B. and G. Narayan (2001), J Environ Biol 22(3): 233-5. Abstract: Freshwater edible catfish Clarias batrachus (Linn.) was treated with sublethal concentration of two different groups of pesticides- carbaryl, a carbamate and phorate, an organophosphate for 24,72,120 and 168 h. The disorders of lipid metabolism were observed in serum. Cholesterol levels in the serum decreased significantly throughout the exposure period with both the pesticides. These results indicate one significant manifestation of the toxic response from the fish under the stress of pesticide exposure. |
| Effect of pH, ionic strength and oxygen burden on the chemical stability of EPC/cholesterol liposomes under accelerated conditions. Part 1: Lipid hydrolysis Zhang, J. A. and J. Pawelchak (2000), Eur J Pharm Biopharm 50(3): 357-64. Abstract: The accelerated stability of purified egg phosphatidylcholine (EPC)/cholesterol liposomes was studied under various formulation conditions using a 2(3) factorial experimental design. The three factors included in the study were pH, ionic strength of the buffer and the headspace oxygen content in the container. The results showed that lipid hydrolysis followed pseudo first-order kinetics. Data analysis using factorial design revealed that pH of the buffer was the predominant factor influencing the rate of lipid hydrolysis. Neither the ionic strength of the buffer, nor the presence of oxygen in the headspace of the container significantly affected the EPC hydrolysis. The hydrolysis rate of EPC at pH 4.0 buffer was at least 1.75 times greater than that at pH 4.8. A prediction based on the Arrhenius equation suggests that the EPC/cholesterol liposomes should be formulated in a buffer with pH equal to or greater than 4. 2 in order to have a shelf-life longer than 1 year at 5 degrees C. |
| Effect of pharmacotherapy on serum cholesterol levels in patients with panic disorder Shioiri, T., K. Fujii, et al. (1996), Acta Psychiatr Scand 93(3): 164-7. Abstract: It is unclear whether elevated cholesterol level is a complication of panic disorder (PD) or is associated with pharmacotherapy. We compared the total cholesterol (TC) level in 47 PD patients with that in 47 gender- and age-matched normal controls (NC), and we also examined the pre- and post-treatment TC levels. There was no sex difference in TC. Before pharmacotherapy, the mean TC level in the PD group (194.9 +/- 39.6 mg/dl) was non-significantly higher than that in the NC group (190.5 +/- 26.7 mg/dl). The mean TC level in the PD group was significantly reduced following the pharmacotherapy (post-TC: 184.7 +/- 31.0 mg/dl; t = 2.44, P < 0.02), and the subgroup treated with alprazolam (n = 26) showed markedly significant decrease of TC after the treatment (t = 2.36, P < 0.03). The TC level in the PD subgroup with agoraphobia (n = 24, 198.9 +/- 37.9 mg/dl) was slightly higher than that in the group without agoraphobia (n = 23, 190.8 +/- 41.6 mg/dl). These findings suggest that there is a relationship between cholesterol levels and treatment in PD. |
| Effect of phosphatidylcholine and cholesterol on pH-sensitive liposomes Hazemoto, N., M. Harada, et al. (1993), Chem Pharm Bull (Tokyo) 41(6): 1003-6. Abstract: We previously reported that liposomes composed of phosphatidylethanolamine (PE) and fatty acid exhibited pH-dependent leakage, aggregation and fusion (N. Hazemoto, M. Harada, N. Komatubara, M. Haga and Y. Kato, Chem. Pharm. Bull., 38, 748 (1990)). In this study, we have examined the effects of phosphatidylcholine (PC) and cholesterol (Chol) on the pH-sensitivity of liposomes. Contents-leakage from liposomes was always accompanied by a change in light-scattering, suggesting that aggregation or fusion of liposomes causes the leakage. The pH-sensitivity was observed only when liposomes contained less than 32 mol% of PC. The leakage vs. pH curves shifted to the more acidic regions as the PC content of the liposomes increased, but the maximum leakage (%) did not change. The effect of cholesterol on the pH-sensitivity depended on the PC/PE ratio of the liposomes. Addition of cholesterol to PC/PE/oleic acid (OA) liposomes system induced two effects, that is, aggregation of liposomes via the reduction in PC content and the stabilization of the liposomal membrane. It was shown that pH-sensitivity can be controlled by addition of the appropriate amount of PC and/or Chol to liposomal lipids. |
| Effect of phosphatidylcholine cholesterol liposomes on the growth of bacterial cultures Mel'iantseva, L. P., V. M. Kreines, et al. (1992), Antibiot Khimioter 37(1): 14-7. Abstract: The in vitro studies showed that incubation of S. aureus, P. aeruginosa, E. coli and P. mirabilis in the presence of phosphatidyl choline cholesterol liposomal suspension was accompanied by inhibited microbial growth. The effect was time- and dose-dependent. The arranged structure of the liposomal membranes played an important role in genesis of the bactericidal action of the liposomes since the use of lipids of the same composition in a nonpolysomal form markedly lowered the bactericidal effect. |
| Effect of phospholipase C on cholesterol solubilization in model bile. A concanavalin A-binding nucleation-promoting factor from human gallbladder bile Pattinson, N. R. and K. E. Willis (1991), Gastroenterology 101(5): 1339-44. Abstract: Human bile contains a phospholipase C activity. To examine its pathophysiological importance, the effect of phospholipase C on the dynamics of lipid solubilization and nucleation (cholesterol crystal formation) were investigated in model bile. Phospholipase C from gallbladder bile from patients with gallstones was partially purified by competitively eluting from a concanavalin A (con A)-Sepharose (Sigma, St. Louis, MO) column and incubating with Pronase (Calbiochem, Behring Diagnostics, La Jolla, CA). Phospholipase C activity was resistant to Pronase digestion. When this fraction (concentrated to half the original volume) was mixed with model bile (1:1, vol/vol), a transfer of cholesterol and phospholipid from the micellar to the vesicular phase and an accelerate nucleation time were found concomitant with phospholipid hydrolysis. These effects were prevented by inhibiting the phospholipase C activity with ethylenediaminetetraacetic acid. To confirm that the results were caused by phospholipase C activity and not some other nucleation-promoting factor within the biliary con A preparation, model bile was incubated with bacterial phospholipase C. An identical cascade of events to that found with the partially purified biliary enzyme was observed. Further purification of the con A-bound proteins on DEAE-Sephadex (Pharmacia, Uppsala, Sweden) did not resolve any separate nucleation-promoting activity to that associated with phospholipase C activity. In conclusion, this study has identified phospholipase C as a/the con A nucleation-promoting activity in human gallbladder bile and has characterized a possible molecular mechanism by which cholesterol nucleation is stimulated by this fraction. |
| Effect of phospholipid fatty acid composition of endothelial cells on cholesterol efflux rates Kilsdonk, E. P., A. N. Dorsman, et al. (1992), J Lipid Res 33(9): 1373-82. Abstract: Human endothelial cells (EA.hy 926 line) were loaded with cationized low density lipoprotein (LDL) and subsequently incubated with fatty acid/bovine serum albumin complexes. The fatty acids were palmitic, oleic, linoleic, arachidonic, and eicosapentaenoic acids. The preincubations resulted in extensively modified fatty acid profiles in cell membrane phospholipids and in cellular cholesteryl esters. The cholesterol efflux from these fatty acid-modified cells was measured using 0.2 mg high density lipoprotein3 (HDL3)/ml medium. The efflux was significantly higher for the palmitic acid-treated cells, compared to all other fatty acid treatments. These differences in efflux rates were not caused by changes in the binding of HDL3 to high affinity receptors on the EA.hy 926 cells. Efflux mediated by dimethyl suberimidate-treated HDL3, which does not interact with high affinity HDL receptors, was similar to efflux induced by native HDL3 after all fatty acid treatments. Our results indicate that high affinity HDL receptors are not important for HDL-mediated efflux of cell cholesterol. The fatty acid composition of the cell membrane phospholipids may be an important determinant. |
| Effect of phospholipids and bile acids on cholesterol nucleation time and vesicular/micellar cholesterol in gallbladder bile of patients with cholesterol stones Jungst, D., T. Lang, et al. (1993), J Lipid Res 34(9): 1457-64. Abstract: Supersaturation and rapid nucleation of cholesterol in bile are of key importance in the pathogenesis of cholesterol gallstones. While the effects of bile acids and phospholipids on cholesterol saturation of bile have been extensively studied, their influence on the cholesterol nucleation time has not been compared. We, therefore, investigated whether increases of bile acid or phospholipid concentrations in bile by in vitro supplementation affect the cholesterol nucleation time. Bile samples were obtained at surgery from patients with cholesterol gallstones. Prior to the nucleation assay the bile samples were divided into 0.5-ml aliquots and supplemented with 1.25, 2.5, 5.0, and 10.0 mumol/ml of different phosphatidylcholines (PC-dimyristoyl, PC-dipalmitoyl, PC-distearoyl, and extracted biliary PCs) or with 5.0, 10.0, and 20.0 mumol/ml of bile acids (glycine or taurine conjugates of cholic acid, deoxycholic acid, or chenodeoxycholic acid). The increase of phosphatidylcholine or bile acid concentration decreased the mean cholesterol saturation index to a similar extent (PC: 0.1-0.3; BA: 0.1-0.2). Supplementations of bile with increasing amounts of synthetic or biliary PCs caused a marked prolongation of the nucleation time in bile from 1.5 +/- 0.2 up to > or = 21 days or 2.5 +/- 0.7 up to > or = 21 days. Concurrently, biliary cholesterol was shifted from vesicles to mixed micelles and the cholesterol/phospholipid ratio of the remaining vesicles was progressively lowered. In contrast, the addition of bile acids to gallbladder bile did not affect the cholesterol nucleation time (2.2 +/- 0.3 days), the percentage of vesicular cholesterol, or the cholesterol/phospholipid ratio of vesicles and micelles.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effect of phospholipids and their molecular species on cholesterol solubility and nucleation in human and model biles Halpern, Z., M. Moshkowitz, et al. (1993), Gut 34(1): 110-5. Abstract: Much research in the pathophysiology of gall stones has been devoted to various molecular species of bile salts. Recent findings have shown the importance of phospholipids in biliary pathophysiology. In the present study the addition of increasing doses of egg lecithin to human and model biles progressively prolonged the nucleation time. Concurrently biliary cholesterol was shifted from the vesicular to the non-vesicular carrier(s) while the cholesterol/phospholipid ratio of the remaining vesicles was progressively lowered. Model bile solutions of identical lipid concentration were prepared using phosphatidylcholine, phosphatidylserine, and phosphatidylethanolamine as the only phospholipid. With phosphatidylethanolamine most of the cholesterol was shifted to the vesicular carrier while phosphatidylserine shifted most of the cholesterol to the non-vesicular carrier(s). With phosphatidylcholine the cholesterol was distributed in both carriers. Phosphatidyl choline species composed of various acyl fatty acids in the sn-1 and sn-2 positions were used as the sole phospholipid in otherwise identical model bile solutions. With palmitic acid in the sn-1 position and arachidonic acid in the sn-2 position most of the cholesterol was found in the non-vesicular carrier. When stearic acid was used in sn-2 position instead of arachidonic acid most of the cholesterol was found in the vesicular carrier. These and other variations in phospholipid molecular species shifted cholesterol among its carriers and also modified the nucleation time of model biles. Most of these effects were also found upon addition of the various phospholipid species to human biles. These findings show the importance of phospholipid species in biliary pathophysiology and may be useful when trying to manipulate cholesterol carriers and solubility in bile. |
| Effect of phytate in soy protein on the serum and liver cholesterol levels and liver fatty acid profile in rats Koba, K., J. W. Liu, et al. (2003), Biosci Biotechnol Biochem 67(1): 15-22. Abstract: Dietary soy protein, in comparison with casein, generally lowers the serum cholesterol concentration in rats fed on a cholesterol-enriched diet, while mixed results were observed in rats fed on a diet free of cholesterol. Soy protein also suppresses the conversion of linoleic acid to arachidonic acid in the rat liver. The present study examines whether phytate, a minor component of a soy protein isolate, is responsible for these beneficial effects of soy protein. Weanling male rats were fed for 4 weeks on a purified diet containing a 20% level of protein (either casein (CAS), soy protein (SOY), phytate-depleted SOY (PDSOY) or phytate-replenished PDSOY (PRSOY)) and cholesterol (0 or 0.5%). The dietary protein source and phytate level only affected the serum and liver cholesterol concentrations when the animals were fed on the cholesterol-enriched diet, being significantly lower in those rats fed on the SOY and PRSOY diets than in those fed on the CAS diet, while the concentrations in the rats fed on the PDSOY diet were intermediate. When the animals were fed on the cholesterol-free diet, the ratio of (20:3n-6 + 20:4n-6)/18:2n-6 in liver phosphatidylcholine, a delta6 desaturation index, was significantly lower in the SOY diet group than in the CAS, PDSOY and PRSOY diet groups. Dietary cholesterol significantly depressed the ratio, but neither depletion nor replenishment of phytate affected the ratio. These results suggest that phytate in soy protein played a limited role in the cholesterol-lowering effect of soy protein and was not involved in the metabolism of linoleic acid. |
| Effect of phytosterols and phytostanols on the solubilization of cholesterol by dietary mixed micelles: an in vitro study Mel'nikov, S. M., J. W. Seijen ten Hoorn, et al. (2004), Chem Phys Lipids 127(2): 121-41. Abstract: The effect of a plant sterol, beta-sitosterol (SI), and a plant stanol, sitostanol (SS), on the solubilization of cholesterol (CH) by model dietary mixed micelles was examined under in vitro conditions with the use of gas chromatography, isothermal titration calorimetry, NMR spectroscopy and cryogenic transmission electron microscopy techniques. Free SI and SS were shown to reduce the concentration of CH in dietary mixed micelles via a dynamic competition mechanism. CH, SI and SS affect the microstructure of lipid vesicles and influence the process of amphiphilic self-assembly of nutrients in the gut with the formation of dietary mixed micelles in a similar manner. Therefore, substitution of CH by phytosterols and phytostanols in the diet does not lead to the notable changes in the mechanism of dietary mixed micelle formation and does not affect the process of the intestinal transport of nutrients and drugs via the micellar diffusion mechanism. Our experimental findings demonstrate that the introduction of plant sterols and plant stanols into the diet is clearly beneficial for the reduction of the intestinal uptake of cholesterol. Due to the limited capacity of dietary mixed micelles to embody hydrophobic sterol/stanol molecules, the micellar concentration of cholesterol is reduced and hence, its transport towards the intestinal brush border membrane decreases. |
| Effect of phytosterols in dietary diacylglycerol on atherosclerosis in cholesterol-fed rabbits Meguro, S., T. Hase, et al. (2003), Nutrition 19(7-8): 670-5. Abstract: OBJECTIVE: The present study investigated the effects of phytosterols (PS) in combination with diacylglycerol (DAG) versus PS in combination with triacylglycerol (TAG) on serum lipids and atherosclerosis in cholesterol-fed rabbits. METHODS: Cholesterol-fed (0.3%) New Zealand white rabbits were treated with a control diet, a 0.3% PS and 7% TAG diet, or a 0.3% PS and 7% DAG diet for 14 wk. RESULTS: Serum total cholesterol level in the PS/DAG group was statistically lower than that in the control and PS/TAG groups, whereas serum high-density lipoprotein cholesterol and triacylglycerol levels were not statistically different between these two groups. The ratio of the atherosclerotic lesion area and the mean thickness of the intima in the aortas of the PS/DAG group were statistically lower than those of the control group, whereas there was no statistical difference between the PS/TAG and control groups. In particular, the ratio of the lesion area in the abdominal aorta and the mean thickness of the intima in the thoracic and total aortas of the PS/DAG group were statistically lower than those of the PS/TAG group. The ratio of the atherosclerotic lesion area and the mean thickness of the intima in the aortas correlated positively with total cholesterol exposure level. CONCLUSIONS: These findings suggested that PS in combination with DAG as opposed to TAG prevents the development of atherosclerosis via a decrease in total cholesterol exposure level and might be useful as a dietary oil for the prevention of atherosclerosis. |
| Effect of phytosterols on cholesterol metabolism and MAP kinase in MDA-MB-231 human breast cancer cells Awad, A. B., H. Williams, et al. (2003), J Nutr Biochem 14(2): 111-9. Abstract: Epidemiological studies suggest that dietary phytosterols may offer protection form some types of cancer including breast cancer. In an attempt to investigate the mechanism by which phytosterols offer this protection, we investigated the effect of the two most common dietary phytosterols, beta-sitosterol and campesterol, on the mevalonate and MAP Kinase (MAPK) pathways in MDA-MB-231 cells. These pathways play a role in cell growth and apoptosis. MDA-MB-231 cell line was used in this study since it is a hormone-insensitive tumor cell line which represents the majority of advanced breast cancer cases. Cells grown in the presence of 16 microM beta-sitosterol or campesterol for 3 days exhibited a 70% and 6% reduction in cell growth, respectively, while cholesterol treatment had no effect on growth as compared to the control. Studies investigating the effect of sterol supplementation on the relative and total sterol composition of cells, showed that cells supplemented with cholesterol contained 23% more cholesterol than the control. Cells supplemented with campesterol had almost one-half the cholesterol of controls but accumulated campesterol to account for 40% of the total sterols. In the case of cells supplemented with beta-sitosterol, cells had only 25% of their sterols as cholesterol and the rest was in the form of beta-sitosterol. All sterols tested equally inhibited de novo cholesterol synthesis using 14C-acetate as substrate. beta-Sitosterol supplemented cells had reduced cholesterol synthesis when using 3H-mevalonolactone as substrate, which suggests that the inhibition in this pathway is downstream of mevalonate where processes such as isoprenylation of proteins may take place. Mevalonate supplementation to cells treated with beta-sitosterol did not completely correct the observed growth inhibition by beta-sitosterol. There was no effect of sterols on the concentrations of both low (21-26 kDa) or high (44-74 kDa) molecular weight isoprenylated proteins in these cells. On the other hand, both the quantity and activity of MAPK was elevated in the cells supplemented with beta-sitosterol. These data suggest that the down regulation of cholesterol synthesis from mevalonate and stimulation of the MAPK pathway may play roles in the inhibition of MDA-MB-231 cell growth by beta-sitosterol. |