| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effect of coffee oil and its unsaponifiable fraction on plasma cholesterol level in female rats al-Kanhal, M. A., F. Ahmed, et al. (1999), Int J Food Sci Nutr 50(2): 99-103. Abstract: The present study was conducted to identify the cholesterol-raising factor in coffee oil besides the other two well-known diterpenes, cafestol and kahweol. Female rats fed coffee oil for 4 weeks showed significantly higher level of plasma cholesterol (P < 0.01) and triacylglycerols (P < 0.01). Feeding unsaponifiable lipids of coffee oil caused significant decrease in plasma cholesterol; however, increase in triacylglycerol was observed. Rats given beta-sitosterol showed increase in plasma triacylglecerol and decrease in cholesterol levels, an effect similar to that observed with unsaponifiable lipids. beta-sitosterol is the major constituent of unsaponifiable lipids of the coffee oil. These results show that cafestol and kahweol diterpene alcohols are not the only cholesterol-raising factors in coffee oil. |
| Effect of coffee on cholesterol and apolipoproteins, corroborated by caffeine levels Sedor, F. A., K. A. Schneider, et al. (1991), Am J Prev Med 7(6): 391-6. Abstract: The possibility that coffee may increase cholesterol levels has created uncertainty among physicians. The confusion arose from cross-sectional studies, in which female coffee drinkers appeared to show a positive association more frequently than men. To clarify this relationship, we designed an intervention trial to reduce caffeine and coffee intake sequentially while measuring total cholesterol and the apolipoprotein A-I and B levels. We conducted the study among women who were coffee drinkers (n = 35) or not coffee drinkers (n = 28). The trial spanned seven months with caffeine-free and coffee-free intervals. Serum caffeine levels corroborated compliance with the dietary protocol. Analysis of the apolipoprotein levels confirms the absence of any influence of coffee on lipoproteins in normocholesterolemic persons. We observed no apparent causal association of coffee or caffeine consumption and cholesterol and apolipoproteins. |
| Effect of colectomy on bile composition, cholesterol crystal formation, and gallstones in patients with ulcerative colitis Harvey, P. R., R. S. McLeod, et al. (1991), Ann Surg 214(4): 396-401; discussion 401-2. Abstract: Bile composition and the presence of cholesterol crystals in bile were studied in bile samples obtained at the time of surgery in patients with ulcerative colitis. Some patients were sampled before colectomy and others at a second operation months to years after a colectomy. Patients in the precolectomy group were found to have bile composition similar to control patients without gallstones, and few had crystals in their bile. In the postcolectomy group, cholesterol concentrations were very high, all biles were supersaturated, and almost all patients had cholesterol crystals in their bile. These findings are similar to those found in persons with cholesterol gallstones. Twenty patients have been followed for at least 3 years after colectomy and to date three have formed cholesterol gallstones. |
| Effect of combination therapy with lipid-reducing drugs in patients with coronary heart disease and "normal" cholesterol levels. A randomized, placebo-controlled trial. Harvard Atherosclerosis Reversibility Project (HARP) Study Group Pasternak, R. C., L. E. Brown, et al. (1996), Ann Intern Med 125(7): 529-40. Abstract: BACKGROUND: Combination drug therapy has been shown to decrease cholesterol levels in hyperlipidemic patients. However, its efficacy has not been well studied in patients previously considered to be normolipidemic, many of whom are now candidates for this therapy. OBJECTIVE: To determine the efficacy and tolerability of multidrug therapy designed to improve low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels in patients with coronary heart disease and average lipid levels. DESIGN: Randomized, placebo-controlled, 2.5-year trial comparing patients receiving usual care with patients receiving stepped-care drug therapy. INTERVENTION: Stepped-care therapy (pravastatin, nicotinic acid, cholestyramine, and gemfibrozil) to decrease total cholesterol levels to less than 4.1 mmol/L (160 mg/dL) and the ratio of LDL cholesterol to HDL cholesterol to less than 2.0. SETTING: 2 academic, urban, tertiary care hospitals. PATIENTS: 91 patients (80 men and 11 women) with coronary heart disease, a mean age of 60 years, total cholesterol levels less than 6.4 mmol/L (250 mg/dL) at baseline, and ratios of total cholesterol to HDL cholesterol greater than 4.0 at baseline. MEASUREMENTS: Fasting serum lipoprotein profile, fasting apolipoprotein levels, and frequency of adverse effects. Patients were assessed every 6 weeks during drug titration and every 3 months thereafter. RESULTS: Mean lipid levels at baseline were as follows: total cholesterol, 5.5 mmol/L (214 mg/dL); LDL cholesterol, 3.6 mmol/L (140 mg/dL); HDL cholesterol, 1.1 mmol/L (42 mg/dL); and triglycerides, 1.8 mmol/L (159 mg/dL). With pravastatin, changes in levels from baseline were -22% for total cholesterol, -32% for LDL cholesterol +8% for HDL cholesterol, and -15% for triglycerides (P < 0.001 for all comparisons). With the addition of 1.5 g of nicotinic acid, additional changes were -6% for total cholesterol (P < 0.002). -11% for LDL cholesterol, +8% for HDL cholesterol, and -10% for triglycerides (P < 0.001 for all comparisons). With 2.25 to 3 g of nicotinic acid, these changes were -7% for total cholesterol (P = 0.007), -14% for LDL cholesterol (P < 0.001), +6% for HDL cholesterol (P = 0.02), and -13% for triglycerides (P = 0.03). With cholestyramine, total cholesterol and LDL cholesterol levels were unchanged compared with the previous step; the change in HDL cholesterol level was -8% (P = 0.03); and the change in triglyceride level was +46% (P < 0.001). With gemfibrozil, total cholesterol level was unchanged; the additional change in LDL cholesterol level was +12% (P = 0.09); the change in HDL cholesterol level was +12% (P = 0.03); and the change in triglyceride level was -37% (P < 0.001). Apolipoprotein B levels decreased by 25% overall (P < 0.001); lipoprotein(a) levels did not change significantly. Adverse effects were primarily attributable to nicotinic acid or cholestyramine. In 18 of the 35 patients (50%) whose baseline LDL cholesterol levels were greater than 3.35 mmol/L (130 mg/dL), pravastatin decreased LDL cholesterol levels to 2.6 mmol/L (100 mg/dL) or less by 6 weeks; 70% of patients needed combination therapy to reach this National Cholesterol Education Program goal during the 2.5 years of the study. Adding nicotinic acid to pravastatin produced LDL cholesterol levels of 2.6 mmol/L or less in 15 more of these 35 patients, so that 94% (n = 33) of the patients receiving these two drugs reached this goal. CONCLUSIONS: To reach current goals for LDL cholesterol levels, most normolipidemic patients with coronary heart disease in this study needed combination therapy. Pravastatin with nicotinic acid and pravastatin with gemfibrozil are well-tolerated combinations that can maintain target LDL cholesterol levels, decrease triglyceride levels, and increase HDL cholesterol levels. Adding resin to these combinations produced no further benefit. |
| Effect of combining psyllium fiber with simvastatin in lowering cholesterol Moreyra, A. E., A. C. Wilson, et al. (2005), Arch Intern Med 165(10): 1161-6. Abstract: BACKGROUND: Soluble fiber supplements are recommended to reduce levels of low-density lipoprotein cholesterol (LDL-C). We evaluated the LDL-C-lowering effect of psyllium husk added to low-dose simvastatin therapy. METHODS: In a 12-week blinded placebo-controlled study, patients were randomized to receive 20 mg of simvastatin plus placebo, 10 mg of simvastatin plus placebo, or 10 mg of simvastatin plus 15 g of psyllium (Metamucil) daily. Levels of total cholesterol, LDL-C, high-density lipoprotein cholesterol, triglycerides, and apolipoprotein B were determined after 4 and 8 weeks of treatment. RESULTS: The study group comprised 68 patients. All treatments were well tolerated, and after 8 weeks the mean LDL-C levels in the group receiving 10 mg of simvastatin plus placebo fell by 55 mg/dL (1.42 mmol/L) from baseline, compared with 63 mg/dL (1.63 mmol/L) in the group receiving 10 mg of simvastatin plus psyllium (P =.03). The mean lowering of LDL-C in the group receiving 20 mg of simvastatin plus placebo was the same as that in the group receiving 10 mg of simvastatin plus psyllium. Similar results were seen for apolipoprotein B and total cholesterol. No significant changes from baseline triglyceride or high-density lipoprotein cholesterol levels occurred. CONCLUSIONS: Dietary psyllium supplementation in patients taking 10 mg of simvastatin is as effective in lowering cholesterol as 20 mg of simvastatin alone. Psyllium soluble fiber should be considered as a safe and well-tolerated dietary supplement option to enhance LDL-C and apolipoprotein B lowering. |
| Effect of community health education on plasma cholesterol levels and diet: the Stanford Five-City Project Fortmann, S. P., C. B. Taylor, et al. (1993), Am J Epidemiol 137(10): 1039-55. Abstract: This paper examines the effects of community-wide health education on diet-related knowledge and behavior and on plasma cholesterol levels during an experimental field study in medium-sized cities in northern California. Samples of the population aged 12-74 years were drawn at baseline and every 2 years thereafter to obtain four cross-sectional surveys; participants aged 25-74 years are included in this paper (n = 6,814 or about 425 per city per survey). The baseline sample was asked to return to three follow-up surveys, also 2 years apart, constituting the cohort survey sample (n = 777). Diet was assessed by 24-hour recalls. In the serial cross-sectional survey samples, nutritional knowledge increased over time in both men and women in all cities; among women, this increase was significantly greater in the treatment cities. Plasma cholesterol declined significantly only in men and in neither sex was there evidence of a larger decline in treatment than in control cities. Dietary saturated fat intake tended to decline, but not significantly in either sex, and there was no evidence of treatment impact. Dietary cholesterol intake declined in both sexes. Results in the cohort samples were similar, except plasma cholesterol levels were unchanged over time in men and increased in women, and dietary saturated fat intake declined significantly among women. Secular improvements in knowledge of nutrition and in dietary cholesterol intake occurred during the early 1980s in both men and women in these four cities, while there was less consistent improvement in dietary saturated fat intake. Only nutritional knowledge among women achieved greater improvement in treatment cities than in control cities. Continued and greater change in nutrition probably requires more sustained effort and broader methods, including changes in the food supply. |
| Effect of community pharmacist intervention on cholesterol levels in patients at high risk of cardiovascular events: the Second Study of Cardiovascular Risk Intervention by Pharmacists (SCRIP-plus) Tsuyuki, R. T., K. L. Olson, et al. (2004), Am J Med 116(2): 130-3. |
| Effect of corn and coconut oil-containing diets with and without cholesterol on high density lipoprotein apoprotein A-I metabolism and hepatic apoprotein A-I mRNA levels in cebus monkeys Stucchi, A. F., L. K. Hennessy, et al. (1991), Arterioscler Thromb 11(6): 1719-29. Abstract: The mechanism(s) by which diets containing corn or coconut oil (31% of energy as fat) totally free of cholesterol or with 0.1% added cholesterol by weight (0.3 mg/kcal) affect plasma high density lipoprotein cholesterol (HDL-C), apoprotein (apo) A-I levels, apo A-I kinetics, and hepatic apo A-I mRNA concentrations were investigated in 26 cebus monkeys. Coconut oil-fed monkeys had elevated levels of plasma total cholesterol (217%), very low density lipoprotein plus low density lipoprotein cholesterol (331%), HDL-C (159%), and apo A-I (117%) compared with corn oil-fed animals. Although the addition of cholesterol to the corn oil diet significantly increased these parameters, no such effects were seen when cholesterol was added to the coconut-oil diet. Both the type of fat and cholesterol in the diet significantly affected HDL apo A-I metabolism by decreasing apo A-I fractional catabolic rate and increasing apo A-I production rate in the coconut oil-fed groups. The decrease in apo A-I fractional catabolic rate in the coconut oil-fed animals was also associated with an increase in the HDL core lipid to surface ratio. Liver apo A-I mRNA abundance was elevated in the coconut oil-fed groups; however, dietary cholesterol had no affect on these levels. The lack of parallel effects of dietary fat and cholesterol on apo A-I production rate and liver apo A-I mRNA levels suggests that the increase in the apo A-I production rate observed in the coconut oil-fed groups resulted from the fat-induced rise in liver apo A-I mRNA abundance, whereas the cholesterol-induced rise in the apo A-I production rate resulted from a mechanism other than changes in liver apo A-I mRNA levels. |
| Effect of cotrimoxazole (Bactrim) on cholesterol metabolism Pugalendi, K. V., S. Ramakrishnan, et al. (1996), Indian J Biochem Biophys 33(2): 141-4. Abstract: Male albino rats when treated with antimicrobial cotrimoxazole (trimethoprim+sulphamethaoxazole) showed an elevation of plasma high density lipoprotein (HDL) cholesterol and lecithin cholesterol acyl transferase activity (LCAT). Very low density lipoprotein and low density lipoprotein (VLDL+S4, 5LDL) cholesterol levels were decreased. However, total blood cholesterol and aortic cholesterol levels were normal. There was decreased synthesis of cholesterol and its content in the liver. Intestinal cholesterol mobilisation (studied using U-14Cglucose) towards lymph was normal in spite of decreased synthesis by intestines. Decreased fecal excretion of bile acids and neutral sterols and normal intestinal contribution may be mainly involved in the blood cholesterol homeostasis. |
| Effect of crilvastatin, a new cholesterol lowering agent, on unesterified LDL-cholesterol metabolism into bile salts by rat isolated hepatocytes Clerc, T., V. Sbarra, et al. (1995), Br J Pharmacol 114(3): 624-31. Abstract: 1. The aim of these experiments was to determine the effect of crilvastatin, a new cholesterol lowering agent, on the metabolism of unesterified low density lipoprotein (LDL)-cholesterol by rat freshly isolated hepatocytes. This preclinical model was developed as an alternative to in vivo experiments, to mimic the metabolic effects of a molecule on its target cells and to define optimal conditions for future experimentation on human hepatocytes. 2. Cells were obtained from normolipidaemic or hypercholesterolaemic rats, hypercholesterolaemia was nutritionally induced. Incubations were performed in a medium containing 600 microM taurocholate and 50 microM or 300 microM crilvastatin. 3. This molecule was shown in vitro to be carried by physiological transporters, i.e., albumin-bile salt micellar associations and LDL. Crilvastatin induced a significance increase in the synthesis and secretion by hepatocytes of bile salts resulting from the metabolism of unesterified LDL-cholesterol in both normolipidaemic and hypercholesterolaemic rats. Stimulation involved non-conjugated as well as tauro- and glyco-conjugated bile salts. These findings corroborate preliminary studies showing in vivo that crilvastatin enhances the secretion of bile acids by stimulating the uptake and incorporation of LDL-cholesterol by the liver. |
| Effect of Cu,Zn superoxide dismutase on cholesterol metabolism in human hepatocarcinoma (HepG2) cells Mondola, P., R. Seru, et al. (2002), Biochem Biophys Res Commun 295(3): 603-9. Abstract: The microsomal enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase and the low density lipoprotein (LDL) receptor pathway carry out a key role on cholesterol homeostasis in eucaryotic cells. The HMG-CoA reductase is sensitive to oxidative inactivation and to phosphorylation by many kinases that are able to inactivate the protein and increase its susceptibility to proteolysis. We previously demonstrated that a calf thymus Cu,Zn SOD affects cholesterol metabolism. This protein binds with rat hepatocyte cell membrane by a specific surface membrane receptor. The involvement of Cu,Zn SOD in cholesterol metabolism is confirmed further by the presence of this antioxidant enzyme in circulating serum lipoproteins. We studied the effect of native human Cu,Zn SOD, metal-free SOD (apo SOD), and SOD-inactivated with hydrogen peroxide on cholesterol metabolism in human hepatocarcinoma HepG2 cells. Results showed that all forms of SODs used, at the concentration of 150 ng/ml, are able to affect cholesterol metabolism decreasing both HMG-CoA reductase activity and its protein levels; this inhibitory effect is accompanied by reduced cholesterol synthesis measured as 14Cacetate incorporation into 14Ccholesterol and by an increased 125ILDL binding to HepG2 cells. Furthermore, the inhibitory effect of Cu,Zn SOD on cholesterol synthesis was completely abolished when the cells were incubated with Cu,Zn SOD in the presence of bisindoilmaleimide (BDM), an inhibitor of protein kinase C (PKC); moreover, we demonstrated that Cu,Zn SOD as well as apo SOD was able to increase PKC activity. Overall, data demonstrate that Cu,Zn SOD affects cholesterol metabolism independently from its dismutase activity and its metal content and that the inhibitory action on cholesterol synthesis is mediated by an activation of protein kinase C. |
| Effect of cyclic estrone sulfate treatment on lipid profiles of postmenopausal women with elevated cholesterol levels Notelovitz, M., S. Katz-Karp, et al. (1990), Obstet Gynecol 76(1): 65-70. Abstract: The effects of two doses of cyclic unopposed estrone sulfate therapy on the lipid profiles of 153 healthy postmenopausal women with baseline total cholesterol levels above 219 mg/dL were compared in a multicenter, double-blind, placebo-controlled study. Patients were assigned randomly to one of three treatment groups: estrone sulfate 0.625 mg (N = 59) or 1.25 mg (N = 43), or placebo (N = 51). The median baseline total cholesterol levels of the three treatment groups were 262, 269, and 262 mg/dL, respectively. Total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), and the HDL/LDL ratio were assessed after 6, 9, and 12 months of treatment. There was a significant monotonic dose-response relationship of estrone sulfate in raising HDL levels, lowering LDL levels, and raising the HDL/LDL ratio at all intervals measured. These results indicate that estrone sulfate is effective in creating a beneficial change in the lipid profile of postmenopausal women with elevated baseline total cholesterol. |
| Effect of cyclodextrin on plasma lipids and cholesterol metabolism in the rat Favier, M. L., C. Remesy, et al. (1995), Metabolism 44(2): 200-6. Abstract: beta-Cyclodextrin (beta-CD) is a bile acid and sterol sequestrant produced by enzymatic modification of starch; this product has the potential to decrease plasma cholesterol. In contrast to the sequestrants having resin- or saponin-like properties, beta-CD is rapidly broken down by the large intestine microflora. beta-CD effects on cecal fermentations and lipid metabolism were thus investigated in rats adapted to semipurified diets containing 0%, 2.5%, or 5% beta-CD. In rats fed beta-CD diets, there was an enlargement of the cecum together with a dramatic increase in the cecal concentration of propionic acid (even with the 2.5% level, in moderately acidic pH conditions). Propionic acid produced in the cecum was readily absorbed and entirely taken up by the liver, whereas there was no significant acetic acid uptake. Dietary beta-CD was highly effective in enhancing bile acid entry into to the cecum: the cecal bile acids pool was 2.2 and 3.6-fold enlarged in rats fed the 2.5% and 5% beta-CD diets, respectively. The solubility percentage of bile acids decreased to approximately 25% in rats fed the beta-CD diets (v 51% in controls); the cecal concentration of soluble bile acids was thus relatively low in these animals. The fecal excretion of steroids was strongly enhanced by beta-CD, and bile acids excretion was practically proportional to the dietary beta-CD level. There was a net lipid-lowering effect of beta-CD, even at the 2.5% level. The effect was more pronounced on triglycerides than on cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effect of cyclosporine on arterial balloon injury lesions in cholesterol-clamped rabbits: T lymphocyte-mediated immune responses not involved in balloon injury-induced neointimal proliferation Andersen, H. O., B. F. Hansen, et al. (1999), Arterioscler Thromb Vasc Biol 19(7): 1687-94. Abstract: Restenosis after balloon dilatation of stenosed coronary arteries is a major clinical problem. Because T lymphocytes occur in neointima and because cyclosporine inhibits T-lymphocyte proliferation, we tested the hypothesis that cyclosporine would attenuate neointimal proliferation after balloon dilation injury. Rabbits with a balloon-injured aorta, randomized to cyclosporine in the human therapeutic range (n=13) or vehicle (n=14) were followed up for 5 weeks; as a control for the effect of cyclosporine, half the rabbits received in addition an aorta allograft. Rabbits were clamped at a human plasma cholesterol level of 5 to 7 mmol/L. Cyclosporine did not affect aorta cholesterol accumulation or neointimal proliferation in balloon-injured aortas; however, it attenuated both in transplanted aortas. Likewise, cyclosporine had no effect on endothelial cells at balloon-injured sites, but protected these cells in the transplanted aortas. Infiltration of smooth muscle cells, T lymphocytes, and macrophages were unaffected by cyclosporine in balloon-injured aortas; however, in transplanted aortas, cyclosporine reduced the relative number of T lymphocytes and macrophages but increased the relative number of smooth muscle cells. Finally, in balloon-injured aortas, cyclosporine did not affect expression of vascular adhesion molecule-1, intercellular adhesion molecule-1, or major histocompatibility complex II, but all these cellular activation markers were attenuated by cyclosporine in transplanted aortas. These results suggest that cyclosporine does not attenuate neointimal proliferation after balloon dilatation, and that T lymphocyte--mediated immune responses are not involved in neointimal proliferation after balloon dilatation. |
| Effect of cyclosporine on HMG-CoA reductase, cholesterol 7alpha-hydroxylase, LDL receptor, HDL receptor, VLDL receptor, and lipoprotein lipase expressions Vaziri, N. D., K. Liang, et al. (2000), J Pharmacol Exp Ther 294(2): 778-83. Abstract: Long-term administration of cyclosporine (CsA) has been shown to cause hypercholesteremia, hypertriglyceridemia, and elevations of plasma low-density and very low-density lipoprotein (LDL and VLDL) levels in humans. This study was undertaken to explore the effects of CsA on expressions of the key lipid regulatory enzymes and receptors. Thus, hepatic expressions of cholesterol 7alpha-hydroxylase (the rate-limiting step in cholesterol conversion to bile acids), LDL receptor, and high-density lipoprotein (HDL) receptor proteins, as well as 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity were determined in rats treated with CsA (18 mg/kg/day) or placebo for 3 weeks. In addition, skeletal muscle and adipose tissue expressions of lipoprotein lipase and VLDL receptor were measured. Western blot analysis was used for all protein measurements using appropriate antibodies against the respective proteins. CsA-treated animals showed mild but significant elevations of plasma cholesterol and triglyceride concentrations. This was associated with a marked down-regulation of cholesterol 7alpha-hydroxylase in the liver and a severe reduction of lipoprotein lipase abundance in skeletal muscle and adipose tissue. However, hepatic LDL receptor and HDL receptor expressions and HMG-CoA reductase activity were not altered by CsA therapy. Likewise, skeletal muscle and adipose tissue VLDL receptor protein expressions were unaffected by CsA administration under the given condition. In conclusion, CsA administration for 3 weeks resulted in a significant reduction of hepatic cholesterol 7alpha-hydroxylase and marked down-regulation of skeletal muscle and adipose tissue lipoprotein lipase abundance in rats. The former abnormality can contribute to hypercholesterolemia by limiting cholesterol catabolism, whereas the latter may contribute to hypertriglyceridemia and VLDL accumulation by limiting triglyceride-rich lipoprotein clearance in CsA-treated animals. |
| Effect of dexamethasone on the expression of high-density lipoprotein binding sites in a culture of rat hepatocytes (independence of hormone effect from intracellular cholesterol pool) Khuang, V., T. G. Vishniakova, et al. (1994), Biull Eksp Biol Med 117(1): 50-3. |
| Effect of dexamethasone palmitate-low density lipoprotein complex on cholesterol ester accumulation in aorta of atherogenic model mice Tauchi, Y., L. Zushida, et al. (2001), Biol Pharm Bull 24(8): 925-9. Abstract: In order to confirm the efficacy of dexamethasone palmitate (DP)-low density lipoprotein (LDL) complex on experimental atherosclerosis in vivo, we examined whether DP-LDL complex could be effective for cholesterol ester accumulation in the aorta of atherogenic mice. Nonatherogenic and atherogenic mice were fed with normal and atherogenic diet for 14 weeks, respectively. Dexamethasone (DEX), lipid emulsion containing DP (DP-LE), or DP-LDL complex was intravenously injected once a week from 8 to 14 weeks. Cholesterol levels in serum and aorta in the atherogenic mice were significantly higher than those of nonatherogenic mice. Injection of DP-LDL complex significantly reduced cholesterol ester (CE) accumulation in the aorta of atherogenic mice. The reduction of CE accumulation in aorta treated with DP-LDL complexes was 10 and 100 times more potent than that with DP-LE and DEX, respectively. The radioactivity in the aorta of atherogenic mice treated with 3H-DP-LDL complex was significantly higher than that with 3H-DP-LE and 3H-DEX at 24 h after injection. Even 7 d after injection, a significant amount of radioactivity was present only in the aorta of atherogenic mice treated with DP-LDL complex. This result suggests that DP-LDL complex is selectively delivered to the atherogenic lesions in the aorta of atherogenic mice, and then DP released from the complex inhibits CE accumulation in the aortic intima. Therefore, DP-LDL complex may be a good drug-carrier in drug delivery system for atherosclerosis. |
| Effect of dexfenfluramine on body weight, blood pressure, insulin resistance and serum cholesterol in obese individuals Holdaway, I. M., E. Wallace, et al. (1995), Int J Obes Relat Metab Disord 19(10): 749-51. Abstract: The effect of the serotonergic agent dexfenfluramine on weight loss, blood pressure, insulin sensitivity and serum lipid levels was determined in a 3-month randomised, double-blind, placebo controlled parallel design study in 50 obese subjects (body mass index 30-44 kg/m2). When compared with placebo treated patients, the dexfenfluramine group lost more weight (3.8 vs 1.1 kg, P < 0.01), had lower diastolic blood pressure (-5 vs -1.5 mmHg, P < 0.05), and lower cholesterol levels (-0.38 vs + 0.06mmol/l, P < 0.05), and showed improved insulin sensitivity (+ 11% vs + 4%, P < 0.03). Significant effects on blood pressure and insulin sensitivity were apparent after 1 week of treatment during which time weight did not change, suggesting a direct effect of the agent independent of weight loss. Dexfenfluramine thus improves a number of cardiovascular risk factors associated with obesity, with benefits additional to those achieved by weight reduction alone. |
| Effect of diet and substrate on the in vitro measurement of cholesterol and fatty-acid synthesis in hepatic tissue of Japanese quail Hood, R. L. (1990), Poult Sci 69(4): 647-51. Abstract: A comparison of acetate, glucose, mevalonate, or water as radioactive substrates for the hepatic synthesis of cholesterol, fatty acids, and glyceride-glycerol was made in Japanese quail fed diets containing either beef fat or tuna oil. The quail fed a diet containing beef fat were fatter and had a significantly higher (P less than.01) concentration of serum cholesterol (5.6 mM per L) than that measured in the serum of quail given tuna oil (4.1 mM per L). Both in vitro cholesterol and fatty-acid synthesis were greater in the quail fed a diet of beef fat than in those fed a diet containing tuna oil. The results showed that mevalonate was the most-suitable radioactive substrate for measuring cholesterol synthesis, whereas glucose was the most-suitable radioactive substrate for measuring fatty-acid and glyceride-glycerol synthesis. |
| Effect of diet on plasma triglycerides, cholesterol, beta-hydroxybutyrate and free fatty acids in cats Dobenecker, B., E. Kienzle, et al. (1998), J Nutr 128(12 Suppl): 2648S-2650S. |