| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effects of pravastatin and ursodeoxycholic acid on cholesterol and bile acid metabolism in patients with cholesterol gallstones Okamoto, S., K. Nakano, et al. (1994), J Gastroenterol 29(1): 47-55. Abstract: To investigate the effects of pravastatin and ursodeoxycholic acid (UDCA) on cholesterol and bile acid metabolism in humans, 41 patients with cholesterol gallstone disease were allocated to four groups and treated with pravastatin (20 mg/day), UDCA (600 mg/day), both pravastatin and UDCA, or neither drug (control) for 1-2 weeks prior to elective cholecystectomy. Cholesterol 7 alpha-hydroxylase activity and serum levels of total 7 alpha-hydroxycholesterol were significantly increased by pravastatin and unaffected by UDCA. 3-Hydroxy-3-methylglutaryl coenzyme A reductase activity was markedly increased by pravastatin and decreased by UDCA. UDCA significantly decreased biliary cholesterol concentration and the cholesterol saturation index and prolonged the nucleation time; however, pravastatin alone had little effect on biliary lithogenicity. Serum total and low-density lipoprotein (LDL)-cholesterol levels were reduced most by the combined administration of pravastatin and UDCA. In conclusion, at a dose of 20 mg/day, pravastatin increased bile acid synthesis but did not decrease biliary lithogenicity. UDCA had no significant effect on bile acid synthesis, but markedly decreased biliary lithogenicity. |
| Effects of pravastatin on cholesterol metabolism in Watanabe heritable hyperlipidemic rabbits Amorosa, L. F., S. J. Rozovski, et al. (1992), Jpn Heart J 33(4): 451-63. Abstract: Pravastatin, a competitive inhibitor of hydroxymethylglutaryl CoA reductase (HMG CoA reductase) is a potent hypocholesterolemic agent in humans as well as experimental animals, including the Watanabe heritable hyperlipidemic (WHHL) rabbit, lacking low density lipoprotein (LDL) receptor activity. We studied the effect of pravastatin on several aspects of cholesterol metabolism in WHHL rabbits. Cholesterol synthesis was measured by intraperitoneal injection of radioacetate and determination of its incorporation into the nonsaponifiable lipid fraction of liver, plasma, adrenal glands and gonads. A single dose of pravastatin (25 mg/kg) caused statistically significant inhibition of hepatic cholesterol synthesis at 2, 6, 12, and 24 hours following oral administration. By 48 hours, the inhibitory effect of the drug was no longer demonstrable. The pattern of radioactivity in the plasma was similar to that in the liver. The drug had no statistically significant effect on cholesterol synthesis in adrenal glands and gonads, suggesting a selective effect on the liver. Cholesterol absorption was studied after simultaneous oral administration of 3H cholesterol and 14C beta-sitosterol. Pravastatin, 50 mg/kg for 10 days had no effect on fecal excretion of the radiolabelled steroids over 4 days. At 24 hours the plasma level of 14C cholesterol was 1/3 that of control in pravastatin treated animals (p < 0.05) but did not undergo an accelerated decline over 6 days. The activity of acyl CoA: cholesterol acyltransferase (ACAT) in intestinal mucosa and the concentration of hepatic cholesterol were similar in animals treated over one year with pravastatin 50 mg/kg/day or with placebo. Our data do not allow us to make definitive conclusions about the effect of pravastatin on cholesterol absorption but are compatible with the hypothesis that the drug inhibits the hepatic synthesis as well as the assembly of cholesterol into lipoproteins. |
| Effects of pravastatin on cholesterol metabolism of cholesterol-fed heterozygous WHHL rabbits Harsch, M., A. Gebhardt, et al. (1998), Br J Pharmacol 124(2): 277-82. Abstract: 1. We administered the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin at a daily dose of 1 mg kg(-1) body weight to cholesterol-fed (0.03%) heterozygous Watanabe heritable hyperlipidaemic rabbits, an animal model for heterozygous familial hypercholesterolaemia. 2. After 12 months of cholesterol treatment, immunohistochemistry with the monoclonal antibody 9D9 was used to detect hepatic low density lipoprotein (LDL) receptors, which were quantified by densitometry. In addition we determined LDL receptor mRNA by competitive reverse transcriptase polymerase chain reaction. The cholesterol precursor lathosterol and the plant sterol campesterol were analysed by gas-liquid chromatography. 3. The drug reduced total plasma cholesterol levels by 51% (P=0.04), when compared to the control group. Unexpectedly, hepatic LDL receptor density and mRNA showed no significant differences between the groups. Total plasma levels of lathosterol and campesterol also revealed no significant differences between the groups, if expressed relative to plasma cholesterol. 4. The findings suggest that mechanisms other than induced hepatic LDL receptors are responsible for the cholesterol-lowering effect of pravastatin in this animal model. We propose a reduced cholesterol absorption efficiency compatible with similar campesterol levels between both groups observed in our study. |
| Effects of pravastatin on coronary events in 2073 patients with low levels of both low-density lipoprotein cholesterol and high-density lipoprotein cholesterol: results from the LIPID study Colquhoun, D., A. Keech, et al. (2004), Eur Heart J 25(9): 771-7. Abstract: AIMS: Fibrates or nicotinic acid are usually recommended for secondary prevention of coronary heart disease in patients with low plasma levels of both low-density lipoprotein cholesterol (LDL-C) < or =140 mg/dL (< or =3.6 mmol/L) and high-density lipoprotein cholesterol (HDL-C) < or =40 mg/dL (< or =1.03 mmol/L). The LIPID trial, a randomised, placebo-controlled trial in 9014 patients at 87 centres in Australia and New Zealand, provided an opportunity to investigate the effects of an HMG-CoA reductase inhibitor in patients with low LDL-C and low HDL-C. METHODS AND RESULTS: Participants in this post hoc substudy were 2073 patients aged 31-75 years with baseline LDL-C < or =140 mg/dL (< or =3.6 mmol/L), HDL-C < or =40 mg/dL (< or =1.03 mmol/L), and triglyceride < or =300 mg/dL (< or =3.4 mmol/L). The relative risk reduction with pravastatin treatment was 27% for major coronary events (95% CI 8-42%), 27% for coronary heart disease mortality (95% CI 0-47%), 21% for all-cause mortality (95% CI 0-38%), and 51% for stroke (95% CI 24-69%). The number needed to treat to prevent a major coronary event over 6 years was 22. CONCLUSIONS: Treatment with pravastatin in patients with both low LDL-C and low HDL-C significantly reduced major coronary events, stroke, and all-cause mortality. The level of HDL-C is crucial to the risk of recurrent CHD events and, consequently, the benefit of lowering LDL-C. |
| Effects of pravastatin on mortality in patients with and without coronary heart disease across a broad range of cholesterol levels. The Prospective Pravastatin Pooling project Simes, J., C. D. Furberg, et al. (2002), Eur Heart J 23(3): 207-15. Abstract: AIMS: To assess the effects of pravastatin on all-cause mortality and cause-specific mortality and to compare the effects for patients with prior coronary heart disease with those for patients without, using pooled data from the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study, the Cholesterol and Recurrent Events (CARE) study, and the West of Scotland Coronary Prevention Study (WOSCOPS). METHODS AND RESULTS: 13 173 patients with coronary heart disease and 6595 men with elevated cholesterol and no prior coronary disease received pravastatin, 40 mg daily, or placebo for an average of 5 to 6 years. Data were analysed according to a pre-specified, published protocol. For all three trials combined, the mortality among patients assigned pravastatin was significantly lower, at 7.9%, than the 9.8% among those assigned placebo, a relative risk reduction of 20% (95% confidence interval (CI) 12-27%, P<0.0001). Active treatment was associated with a reduction in coronary mortality (24%, 95% CI 14-33%). Larger reductions in absolute risk were estimated in those with prior coronary heart disease than in those without. CONCLUSION: Treatment with pravastatin over 5 years reduces all-cause mortality and coronary mortality in patients with and those without a history of coronary heart disease. The size of the benefit was related principally to the baseline risk. |
| Effects of pregnenolone-16 alpha-carbonitrile on the metabolism of cholesterol in rat liver microsomes Stahlberg, D. (1995), Lipids 30(4): 361-4. Abstract: The effects of pregnenolone-16 alpha-carbonitrile (PCN) on hepatic metabolism of cholesterol were studied in rat liver microsomes in order to clarify the underlying mechanisms of the PCN-induced biliary hypersecretion of cholesterol. Male Sprague-Dawley rats were fed a diet supplemented with 0.05% of PCN for one week. The microsomal activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, regulating cholesterol biosynthesis, decreased from 577 +/- 46 (SEM) to 367 +/- 38 pmol/min/mg protein compared to the controls. Cholesterol 7 alpha-hydroxylase activity, governing bile acid synthesis, was 9.0 +/- 1.1 pmol/min/mg protein in the treated group and 34.8 +/- 7.4 pmol/min/mg protein in the controls, a reduction of 74% (P < 0.01). The acyl CoA:cholesterol acyltransferase (ACAT) activity, catalyzing the esterification of cholesterol, remained unchanged, as did the levels of total and free cholesterol in liver homogenates and microsomes. The results of this study provide evidence that the increase in biliary cholesterol secretion during PCN treatment is not caused by a change in ACAT activity, but can be explained by a decreased catabolism of cholesterol to bile acids. |
| Effects of probucol and pravastatin on plasma lipids, activities of postheparin lipoprotein lipase, and lecithin cholesterol acyltransferase and apo A-I containing lipoproteins with and without apo A-II in patients with moderate hypercholesterolemia Kagami, A., T. Ishikawa, et al. (1993), Clin Biochem 26(2): 101-7. Abstract: In this study, plasma HDL fractions were separated by ultracentrifugation and apo A-I containing lipoproteins (A-I Lp) were then isolated using anti-apo A-I immunoaffinity chromatography. The A-I Lp were further separated into two fractions with the use of anti-apo A-II immunoaffinity chromatography. One fraction, Lp A-I, contained apo A-I without apo A-II, while the other, Lp A-I/A-II, contained both apo A-I and apo A-II. These techniques were applied to investigate the changes in HDL apoprotein composition in hypercholesterolemic subjects treated with either probucol or pravastatin. Treatment with probucol (500 mg/day) or pravastatin (10 mg/day) reduced mean plasma total cholesterol concentrations by 24% (p < 0.01) and 16% (p < 0.05), respectively. Both drugs caused some reduction in lipoprotein lipase activity, but neither had any influence on the activity of hepatic triglyceride lipase or lecithin cholesterol acyltransferase. Their effects on HDL-cholesterol levels and apoprotein composition differed markedly. Probucol significantly decreased the HDL-cholesterol concentration, the plasma apo A-I/apo A-II ratio, and the number of large particles of diameter greater than 10.4 nm. When the ratios of Lp A-I and Lp A-I/A-II for the probucol-treated subjects were compared with those in the normolipidemic controls, and with the ratios before and after administration of probucol, a remarkable decrease in the level of Lp A-I was apparent. It is presumed that the decrease in HLD-cholesterol by prolonged probucol administration reflects the decrease of Lp A-I more than the decrease of Lp A-I/A-II.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effects of probucol on cholesterol metabolism in mouse peritoneal macrophages: inhibition of HDL-mediated cholesterol efflux Takemura, T., M. Sakai, et al. (2000), Atherosclerosis 152(2): 347-57. Abstract: Macrophage-derived foam cells are known to play an essential role in the development and progression of atherosclerotic lesions. Probucol prevents oxidative modification of low-density lipoprotein (LDL) and lowers plasma contents of LDL and high-density lipoprotein (HDL). A recent report using apoE -/- mice demonstrated that probucol treatment enhanced atherosclerosis in apoE -/- mice more rapidly than that in untreated apoE -/- mice, and a reduction in plasma cholesterol by probucol was not the cause of enhancement of atherosclerotic lesions in probucol-treated apoE -/- mice. Moreover, probucol was reported to inhibit apoA-I mediated cholesterol efflux from mouse macrophages. These reports suggested that probucol might directly affect cholesterol metabolism in mouse macrophages. Thus, we investigated the effects of probucol on cholesterol metabolism in mouse resident peritoneal macrophages. Probucol did not affect degradation of acetylated LDL (Ac-LDL), degradation of LDL and endogenous cholesterol synthesis in mouse macrophages. However, it significantly inhibited HDL-mediated cholesterol efflux. Moreover, probucol partially (30%) inhibited the binding of HDL to mouse macrophages, and significantly activated acyl-coenzyme A:cholesterol acyltransferase (ACAT). Our results suggested that probucol inhibited HDL-mediated cholesterol efflux by inhibiting the binding of HDL to mouse macrophages and reducing HDL-accessible free cholesterol content by ACAT activation, thereby worsening atherosclerotic lesions in apoE -/- mice. However, it remains unclear whether probucol inhibits HDL-mediated cholesterol efflux from human macrophages. |
| Effects of probucol on renal function and urinary protein excretion in spontaneously hypercholesterolemic rats fed a normal or high cholesterol diet Nakao, A., K. Nosaka, et al. (2004), Kidney Blood Press Res 27(2): 96-104. Abstract: BACKGROUND/AIM: Spontaneously hypercholesterolemic (SHC) rats develop hypercholesterolemia and focal glomerular sclerosis, and have been thought to be a model of lipid-induced glomerular injury. However, recent studies suggest that the hypercholesterolemia might be due to secondary mechanisms by massive proteinuria. The purpose of the present study was to determine in SHC rats the effects of a high cholesterol diet on serum lipid profiles and renal function/histology, and to examine whether or not the model of lipid-induced renal injury could be developed in a short period of the time. The effects of probucol were also studied. METHODS: SHC rats were fed a high cholesterol diet for 6 weeks (H) or with probucol (HP), while control SHC rats were fed normal rat chow (N) or with probucol (P). Lipid profile and renal function/histology were examined. RESULTS: H and HP showed increased levels of urinary protein excretion and serum creatinine, as well as extremely high serum cholesterol levels, compared with N and P. HP tended to show reduced urinary protein excretion compared with H, but the difference was not statistically significant. H and HP presented histologically characteristic changes with numerous foam cells accumulated in the glomerular mesangial area, and showed glomerular sclerosis. CONCLUSION: The data demonstrate that SHC rats have an intrinsically abnormal lipid metabolism, and that probucol does not exert obviously beneficial effects on renal function or lipid-lowering action. A lipid-induced renal injury model of rats was produced in 6 weeks. |
| Effects of prolactin on DNA biosynthesis, cholesterol content, and steroidogenesis in the adrenal cortex of guinea pigs treated with dexamethasone Sautin, I., E. I. Kovzun, et al. (1997), Biull Eksp Biol Med 123(1): 18-21. |
| Effects of prolonged ACTH-stimulation on adrenocortical cholesterol reserve and apolipoprotein E concentration in young and aged Fischer 344 male rats Cheng, B., S. C. Chou, et al. (1998), J Steroid Biochem Mol Biol 66(5-6): 335-45. Abstract: Changes in the morphology of rat adrenal cortex with age include increased accumulations of lipid droplets and lipofuscin granules. Because glandular concentrations of cholesteryl esters (CE) and apolipoprotein (apo) E are also increased in parallel, the utilization or metabolism of lipid-droplet stored CE for steroidogenesis might be altered in aging cells. To explore this possibility, adrenocortical cholesterol storage and utilization were studied in 3-6 months-old (mo) (Y) rats and 20-23 mo (O) Fischer 344 male rats. Both groups received either adrenocorticotropin (ACTH1-39, Acthar gel) or gelatin alone daily for seven consecutive days. We found that: (a) the CE concentration in O rats, but not Y animals, was diminished by ACTH. The depleted CE in stimulated-O rats was replenished within five days post stimulation. Failure to deplete CE in stimulated-Y rats was not associated with an insufficient dose of the hormone, since stimulation of Y animals with higher doses of ACTH actually increased the CE concentration. In contrast, adrenocortical free cholesterol concentration remained constant during stimulation regardless of age. (b) The depleted CE in stimulated-O rats was principally comprised of cholesteryl adrenate, cholesteryl arachidonate and cholesteryl cervonate. The accumulated CE in stimulated-Y animals was primarily comprised of cholesteryl adrenate, cholesteryl arachidonate and cholesteryl oleate. (c) Whereas in stimulated-Y rats adrenal apoE concentration declined, the concentration in stimulated O animals was well maintained. (d) In vitro, adrenal homogenate or cytosolic fraction from stimulated-O rats displayed a higher capacity to hydrolyze exogenous CE than its Y counterpart. However, cholesterol esterification with external fatty acid substrates in adrenal homogenate or microsomal fraction was comparable in the two age-groups. Our findings revealed altered adrenocortical cholesterol reserve in O rats to cope with prolonged ACTH-stimulation. Changes in apoE levels and CE hydrolysis activity may be factors associated with this alteration. Depletion and accumulation of adrenocortical CE are reflected in parallel changes in cholesteryl adrenate and cholesteryl arachidonate, suggesting physiologic importance of these polyunsaturated fatty acids during sustained steroidogenesis. |
| Effects of prolonged administration of lovastatin, an inhibitor of cholesterol synthesis, on the morphology and function of rat Leydig cells Andreis, P. G., L. Cavallini, et al. (1990), Exp Clin Endocrinol 96(1): 15-24. Abstract: We examined the effects of a prolonged treatment with lovastatin, a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on the morphology and function of rat Leydig cells. Twenty-four h after the first lovastatin injection, no conspicuous ultrastructural changes were found, but isolated Leydig cells showed a notable reduction in their basal and HCG-stimulated testosterone production. By prolonging lovastatin administration (daily injections for 3 and 5 days), Leydig cells progressively recovered their secretory activity, and this was associated with a striking proliferation of smooth endoplasmic reticulum and peroxisomes. The hypothesis is discussed that these morphologic changes are the counterpart of an enhanced newly synthesis of HMG-CoA reductase, that is the expression of a compensatory response of Leydig cells aimed at maintaining an adequate production of cholesterol (i.e. testosterone precursors) in spite of the chronic competitive inhibition of HMG-CoA reductase by lovastatin. |
| Effects of prospective, randomized cholesterol-lowering dietary intervention and apolipoprotein E phenotype on serum lipoprotein(a) concentrations of infants aged 7-24 mo Routi, T., T. Ronnemaa, et al. (1996), Am J Clin Nutr 63(3): 386-91. Abstract: A high serum lipoprotein(a) Lp(a) concentration is associated with increased risk of coronary artery disease. Few external factors are able to markedly modify serum Lp(a) concentrations. The aim of this study was to evaluate how serum Lp(a) concentrations of infants between 7 and 24 mo of age change in a cholesterol-lowering dietary intervention, and to assess the influence of apolipoprotein (apo) E phenotypes on serum Lp(a) concentrations. The intervention children (n=394) had serum cholesterol, non-high-density-lipoprotein cholesterol, and cholesterol corrected for Lp(a)-cholesterol values (P for all <0.001) lower than those of the control children (n=390), but median serum Lp(a) concentrations at the age of 24 mo were not different from those of control children. Serum Lp(a) values differed according to the apo E phenotype as the median Lp(a) values increased from E2/2 to E3/2, E4/2, E3/3, E4/3, and to E4/4 (P for the difference=0.023, Mann-Whitney U test). Our results suggest that apo E phenotype influences serum Lp(a) concentrations noticeably, but the effect of the cholesterol-lowering dietary intervention was not significant in subjects aged 24 mo. |
| Effects of protein source and amino acid supplementation on plasma cholesterol in guinea pigs Atwal, A. S., S. Kubow, et al. (1997), Int J Vitam Nutr Res 67(3): 192-5. Abstract: The effects of three dietary protein treatments were compared on cholesterol content of plasma lipoprotein fractions and oxidative status of liver lipids in adult guinea pigs. All diets were adequate in soluble dietary fiber and well-balanced in fatty acids providing 30% of total energy. After seven weeks dietary treatments, casein compared to soy protein increased cholesterol in a sub-fraction of LDL (low density lipoprotein) with larger molecular weight and in a combination of this sub-fraction of LDL plus VLDL (very low density lipoprotein) taken together. Supplementation of casein diet with glycine, alanine, arginine and cystine tended to decrease cholesterol in the sub-fraction of LDL with larger molecular weight. There was no effect of dietary treatments on thiobarbituric acid reactive substances in lipids extracted from guinea pig liver likely due to the very high vitamin E and C content of the diets. In addition to counteracting the serum cholesterol elevating effects of dietary cholesterol soy protein also appears to attenuate the hypercholesterolemic effects of dietary saturated fatty acids. |
| Effects of psyllium hydrophilic mucilloid on LDL-cholesterol and bile acid synthesis in hypercholesterolemic men Everson, G. T., B. P. Daggy, et al. (1992), J Lipid Res 33(8): 1183-92. Abstract: The goal of the current study was to determine the mechanism of the hypocholesterolemic effect of psyllium using a randomized, double-blind, crossover design. Twenty males (age 44 +/- 4 yr, weight 79 +/- 10 kg) with moderate hypercholesterolemia (total 265 +/- 17 mg/dl, low density lipoprotein (LDL) 184 +/- 15 mg/dl) were studied at baseline (B) and after randomization to receive a 40-day course of 15 g/day of either psyllium (Ps) or placebo (Pl) (cellulose). After a washout period (11 +/- 2 days), subjects were crossed over to the other fiber treatment for an additional 40 days and restudied. Intestinal cholesterol absorption, cholesterol synthesis in isolated peripheral blood mononuclear cells, bile acid kinetics, gallbladder motility, and intestinal transit were measured at each study period. Psyllium lowered LDL cholesterol (x:184 (B), 169 (Ps), and 179 (Pl) mg/dl; Ps vs. B,Pl: P less than 0.004, P less than 0.02), decreased relative cholesterol absorption (x:51 (B), 45 (Ps), and 49 (Pl) %; Ps vs. B,Pl: P less than 0.03, P less than 0.03), did not alter absolute cholesterol absorption, and increased the fractional turnover of both chenodeoxycholic acid (x:0.176 (B), 0.203 (Ps), and 0.170 (Pl) day-1; Ps vs. B,Pl: P less than 0.0001, P less than 0.01) and cholic acid (x:0.303 (B), 0.411 (Ps), and 0.301 (Pl) d-1; Ps vs. B, Pl: P less than 0.006, P less than 0.002). Bile acid synthesis increased in subjects whose LDL cholesterol was lowered by more than 10% (Ps vs. B: 1304 +/- 489 vs 992 +/- 307 mumol/day, P less than 0.006; Ps vs. PI: 1304 +/- 489 vs. 914 +/- 321 mumol/day, P less than 0.0002). We conclude that psyllium lowers LDL cholesterol primarily via stimulation of bile acid synthesis. |
| Effects of psyllium on plasma total and lipoprotein cholesterol and hepatic cholesterol in hamsters fed n-3 PUFA or n-6 PUFA with high cholesterol levels Liu, Y. C., S. Y. Liu, et al. (2004), Ann Nutr Metab 48(6): 374-80. Abstract: This study was conducted to determine whether psyllium is known to alter cholesterol metabolism modulate the hypercholesterolemic effect of a high cholesterol, n-3 polyunsaturated fatty acids (PUFA) diet in hamsters. Concentrations of plasma, hepatic total cholesterol and lipoprotein cholesterol were measured in male hamsters fed an n-3 PUFA plus psyllium (8%, wt/wt) diet combined with variable levels of cholesterol (0, 0.05, 0.1%, wt/wt) or a cholesterol-enriched (0.2%, wt/wt) n-3 PUFA or n-6 PUFA diet that contained either 8% methyl cellulose or psyllium for 4 weeks. In the n-3 PUFA-fed hamsters, we have found that psyllium was able to reduce plasma total cholesterol and low density lipoprotein (LDL)-cholesterol significantly when 0.1% cholesterol was added to the diet. In contrast, the effects of psyllium were not seen in the n-3 PUFA-fed hamsters without dietary cholesterol or with 0.05% dietary cholesterol. However, no matter in the presence of psyllium or not, the increase of plasma total cholesterol, very-low-density lipoprotein (VLDL)-cholesterol, LDL-cholesterol and high-density lipoprotein (HDL)-cholesterol levels was depend on the content of dietary cholesterol. Although the cholesterol diet increased the liver total cholesterol level, 80 g psyllium/kg diet resulted in a significantly lower concentration of liver total cholesterol in the cholesterol-fed hamsters. In the second experiment, we have also found that psyllium feeding lowered significantly plasma total cholesterol and VLDL-cholesterol concentrations in hamsters fed n-3 PUFA but not in those fed n-6 PUFA. However, the levels of plasma total cholesterol, VLDL-cholesterol and LDL-cholesterol levels of the (n-6) PUFA-fed hamsters were significantly lower than those in the (n-3) PUFA-fed hamsters in the absence or presence of dietary psyllium. Our data also showed that hamsters fed both high-cholesterol n-3 PUFA and n-6 PUFA diets had a significant decrease in hepatic cholesterol with intake of psyllium. Liver total cholesterol concentrations were significantly lower in n-3 PUFA-fed hamsters compared with the n-6 PUFA-fed groups. Therefore, these data may contribute to understanding the interactive effect of psyllium and cholesterol or the type of fat on plasma and liver cholesterol in hamsters. |
| Effects of qigong on blood pressure, high-density lipoprotein cholesterol and other lipid levels in essential hypertension patients Lee, M. S., M. S. Lee, et al. (2004), Int J Neurosci 114(7): 777-86. Abstract: This study investigated the effectiveness of Qigong on blood pressure and several blood lipids, such as high-density lipoprotein (HDL) cholesterol, Apolipoprotein A1 (APO-A1), total cholesterol (TC), and triglycerides (TG) in hypertensive patients. Thirty-six patients were randomly divided into either the Qigong group, or a wait-listed control group. Blood pressures decreased significantly after eight weeks of Qigong. The levels of TC, HDL, and APO-A1 were changed significantly in the Qigong group post-treatment compared with before treatment. In summary. Qigong acts as an antihypertensive and may reduce blood pressure by the modulation of lipid metabolism. |
| Effects of Quillaja saponins on growth, metabolism, egg production and muscle cholesterol in individually reared Nile tilapia (Oreochromis niloticus) Francis, G., H. P. Makkar, et al. (2001), Comp Biochem Physiol C Toxicol Pharmacol 129(2): 105-14. Abstract: The effects of supplementation of a Quillaja saponin (QS) mixture in the diets of tilapia have been studied using a respirometer system that allowed feeding and continuous measurement of oxygen consumption of individual fish. Five fish each were given control diet (C group) and control diet supplemented with 150 mg kg(-1) (S150 group) or 300 mg kg(-1) (S300 group) QS. At the end of 14 weeks the weight gain of the S300 group was significantly higher than control (P<0.05) whereas that of the S150 group had an intermediate value. The S150 group had a higher growth rate (P=0.05) after the first 3 weeks of feeding with the experimental diets, compared to the other two groups. At the end of the experiment the S300 group had significantly higher (P<0.05) average values for energy retention, apparent lipid conversion, carcass fat, energy and significantly lower (P<0.05) average values for apparently unutilised energy and carcass ash content compared to the C group. The corresponding values of the S150 group were intermediate between the C and S300 groups. One out of two female fish in the S150 group and both female fish in the S300 group never produced eggs during the entire 14-week experimental period. Contrarily, all three female fish in the control group and one out of the two female fish in the S150 group regularly produced eggs, at a rate of approximately once in every 14 days. The muscle cholesterol level in the S300 group was significantly higher than that of the C group. Possible mechanisms of action of the dietary saponins are discussed. |
| Effects of radiation on the longitudinal trends of total serum cholesterol levels in the atomic bomb survivors Wong, F. L., M. Yamada, et al. (1999), Radiat Res 151(6): 736-46. Abstract: The effects of radiation on the long-term trends of the total serum cholesterol levels of the Hiroshima and Nagasaki atomic bomb survivors were examined using data collected in the Adult Health Study over a 28-year period (1958-1986). The growth-curve method was used to model the longitudinal age-dependent changes in cholesterol levels. For each sex, temporal trends of cholesterol levels were characterized with respect to age, body mass index, city and birth year. We then examined whether the temporal trends differed by radiation dose. We showed that the mean growth curve of cholesterol levels for the irradiated subjects were significantly higher than that for the unirradiated subjects, and that the increase was greater for women than for men. No difference in dose response was detected between Hiroshima and Nagasaki. An increased mean level of cholesterol was evident for irradiated women in general, but a notable increase was apparent in males only for the youngest birth cohort of 1935-1945. The difference in the mean cholesterol levels between the irradiated and unirradiated subjects diminished past 70 years of age. It is not known whether this is due to natural progression or is an artifact of nonrandom variation in the rate of participation in the examinations. The maximum predicted increase at 1 Gy for women occurred at age 52 years for the 1930 cohort: 2.5 mg/dl (95% CI 1.6-3.3 mg/dl) for Hiroshima and 2.3 mg/dl (95% CI 1.5-3.1 mg/dl) for Nagasaki. The corresponding increase for men occurred at age 29 years for the 1940 cohort: 1.6 mg/dl (95% CI 0.4-2.8) for Hiroshima and 1.4 mg/dl (95% CI 0.3-2.6) for Nagasaki. Controlling for cigarette smoking did not alter the dose-response relationship. Although the difference in the mean growth curves of the irradiated and unirradiated groups was statistically significant, there was a considerable overlap in the individual growth curves of the two groups. The significant sex difference and the greater magnitude of radiation effects in women suggest that hormonal changes resulting from radiation exposure, such as accelerated menopause, is an area worth investigating to delineate the mechanisms underlying the increased cholesterol levels of the irradiated female subjects. This increase may also partially explain the increased rate of coronary heart disease seen in the atomic bomb survivors. |
| Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women Delmas, P. D., N. H. Bjarnason, et al. (1997), N Engl J Med 337(23): 1641-7. Abstract: BACKGROUND: Long-term estrogen therapy can reduce the risk of osteoporotic fracture and cardiovascular disease in postmenopausal women. At present, however, these beneficial effects are not separable from undesirable stimulation of breast and endometrial tissues. METHODS: We studied the effect of raloxifene, a nonsteroidal benzothiophene, on bone mineral density, serum lipid concentrations, and endometrial thickness in 601 postmenopausal women. The women were randomly assigned to receive 30, 60, or 150 mg of raloxifene or placebo daily for 24 months. RESULTS: The women receiving each dose of raloxifene had significant increases from base-line values in bone mineral density of the lumbar spine, hip, and total body, whereas those receiving placebo had decreases in bone mineral density. For example, at 24 months, the mean (+/-SE) difference in the change in bone mineral density between the women receiving 60 mg of raloxifene per day and those receiving placebo was 2.4+/-0.4 percent for the lumbar spine, 2.4+/-0.4 percent for the total hip, and 2.0+/-0.4 percent for the total body (P<0.001 for all comparisons). Serum concentrations of total cholesterol and low-density lipoprotein cholesterol decreased in all the raloxifene groups, whereas serum concentrations of high-density lipoprotein cholesterol and triglycerides did not change. Endometrial thickness was similar in the raloxifene and placebo groups at all times during the study. The proportion of women receiving raloxifene who reported hot flashes or vaginal bleeding was not different from that of the women receiving placebo. CONCLUSIONS: Daily therapy with raloxifene increases bone mineral density, lowers serum concentrations of total and low-density lipoprotein cholesterol, and does not stimulate the endometrium. |