| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| The effect of feeding lovastatin and colestipol on production and cholesterol content of eggs Luhman, C. M., B. G. Miller, et al. (1990), Poult Sci 69(5): 852-5. Abstract: The purpose of the present study was to determine whether feeding lovastatin or colestipol, or both, to laying hens would decrease the concentration of cholesterol in eggs. Forty-eight White Leghorn hens (69 wk of age) were allocated randomly to one of four groups. For 5 wk, the birds were fed: 1) a control diet; 2) diets supplemented with 35 mg of lovastatin per kg of feed; 3) 11.7 g of colestipol per kg of feed; or 4) both 35 mg of lovastatin and 11.7 g of colestipol per kg of feed. Drug feeding did not affect egg production or the concentration of cholesterol in the yolk, muscle, or liver. Lovastatin residue was found in liver samples from hens receiving lovastatin, but no lovastatin residue was found in the muscle, egg-white, or egg-yolk samples from hens on any treatment. These findings suggest that lovastatin or colestipol, or both, fed at relatively low amounts do not decrease the concentration of cholesterol in egg yolk and do not depress egg production. |
| The effect of fibric acid derivatives on cholesterol metabolism in rat liver Shand, J. H. and D. W. West (1994), Biochem Soc Trans 22(2): 110S. |
| The effect of fish oil on blood pressure and high-density lipoprotein-cholesterol levels in phase I of the Trials of Hypertension Prevention. Trials of Hypertension Prevention Collaborative Research Group Sacks, F. M., P. Hebert, et al. (1994), J Hypertens Suppl 12(7): S23-31. Abstract: OBJECTIVE: To study the effects of moderate doses of fish oil on blood pressure and high-density lipoprotein (HDL)-cholesterol. METHODS: The participants were 350 normotensive men and women aged 30-54 years who were enrolled from seven academic medical centers in phase I of the Trials of Hypertension Prevention. They were randomly assigned to receive placebo or 6 g purified fish oil once a day, which supplied 3 g n-3 polyunsaturated fatty acids for 6 months. RESULTS: Baseline blood pressure was (mean +/- SD) 123 +/- 9/81 +/- 5 mmHg. The mean differences in the blood pressure changes between the fish oil and placebo groups were not statistically significant. There was no tendency for fish oil to reduce blood pressure more in subjects with baseline blood pressures in the upper versus the lower quartile (132/87 versus 114/75 mmHg), low habitual fish consumption (0.4 versus 2.9 times a week) or low baseline plasma levels of n-3 fatty acids. Fish oil increased HDL2-cholesterol significantly compared with the placebo group. Subgroup analysis showed this effect to be significant in the women but not in the men. Increases in serum phospholipid n-3 fatty acids were significantly correlated with increases in HDL2-cholesterol and decreases in systolic blood pressure. CONCLUSION: Moderate amounts of fish oil (6 g/day) are unlikely to lower blood pressure in normotensive persons, but may increase HDL2-cholesterol, particularly in women. |
| The effect of ginseng on bile-pancreatic secretion in the rat. Increase in proteins and inhibition of total lipids and cholesterol secretion Salam, O. M., S. A. Nada, et al. (2002), Pharmacol Res 45(4): 349-53. Abstract: Ginseng is one of the most popular herbal remedies. Studies were performed in anaesthetized rats to examine the effect of ginseng on bile secretion. Male Sprague-Dawley rats were anaesthetized with intraperitoneal (i.p.) urethane (1.25 g kg(-1)) and equipped with biliary cannulas inserted into the bile duct through the sphincter of Oddi. Rats were treated with a single i.p. injection of ginseng at 25, 50 or 100 mg kg(-1) (1 ml(-1)) 30 min before bile collection; the control group received i.p. saline only at 1 ml(-1)volume. The effect of multiple doses of ginseng on bile volume and biliary composition was also studied. Ginseng was given in the higher dose of 100 mg kg(-1) (1 ml(-1), i.p.) every 12 hours for 2 days. Bile was collected in 15 min fractions for 90 min. Bile flow (bile-pancreatic juice), biliary excretion of total proteins, cholesterol and total lipids were measured. The single administration of different doses (25, 50 and 100 mg kg (-1)) of ginseng reduced basal bile secretion in a dose-dependent manner. Single-dose administration of ginseng at 100 mg kg(-1) caused 32.9% reduction in basal bile flow. Meanwhile, mean basal bile flow was reduced by 15.1% in rats treated with multiple doses of ginseng at 100 mg kg(-1) for two days. Biliary protein concentrations were significantly increased after single- or multiple-dose administration of ginseng, but protein output was only significantly increased (33%) in rats treated with ginseng (100 mg kg(-1)) twice a day for 2 days. Biliary total lipids and cholesterol concentration and outputs were significantly reduced after single or multiple administration of ginseng. In conclusion, administration of ginseng in the rat resulted in a reduction of bile flow and in bile secretion of total lipids and cholesterol, while it increased the secretion of proteins in a dose-dependent manner. The precise mechanisms underlying these effects remain to be elucidated. The findings indicate the need for clinical trials for the effect of this herb on bile composition and flow in man in view of a possible modulatory effect for the herb on gallstone formation. |
| The effect of glycemic control and duration of diabetes on cholesterol and phospholipid classes in erythrocytes of type I diabetes Jain, S. K., R. McVie, et al. (1992), Metabolism 41(3): 285-9. Abstract: Abnormalities in the lipid composition of erythrocytes can alter blood rheology and viscosity. These alterations have been implicated in the pathogenesis of microvascular disease in diabetic patients. The present study was undertaken to examine whether or not long-term glycemic control or duration of diabetes has any role in the altered membrane cholesterol and phospholipid composition of erythrocytes in type I diabetes. Long-term glycemic control was assessed by measuring glycosylated hemoglobin (GHb) from diabetic patients and age-matched normal volunteers. There was no significant correlation between GHb or duration of diabetes with total cholesterol, phospholipid, and cholesterol to phospholipid molar ratios in erythrocytes of these patients. Among phospholipid classes, GHb showed a significantly negative relationship with sphingomyelin (SM) (r =.55, P less than.01) levels, but was not related to phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels of erythrocytes. Duration of diabetes had no effect on SM, PC, or PE levels of erythrocytes. |
| The effect of growth hormone on low-density lipoprotein cholesterol and lipoprotein (a) levels in familial hypercholesterolemia Tonstad, S., E. Sundt, et al. (1996), Metabolism 45(11): 1415-21. Abstract: Severe elevations of low-density lipoprotein (LDL) cholesterol are not always normalized with conventional drugs. Growth hormone decreases LDL cholesterol levels, in part by augmenting liver LDL receptor activity. This increase may be on the order of magnitude of the increase induced by statins. We investigated the effect of growth hormone in familial hypercholesterolemia (FH) in a randomized, double-blind, placebo-controlled study. Thirty-one men with FH aged 20 to 48 years, of whom 81% had a known LDL receptor gene mutation, discontinued all lipid-lowering drugs 6 weeks before the study. Dietary stabilization continued for 5 more weeks, followed by single-blind placebo injections for 1 week. Thereafter, 16 subjects were allocated to recombinant growth hormone 0.05 IU/kg/d and 15 to placebo injected subcutaneously for 12 weeks. Baseline lipid levels were similar in both groups. One subject in the growth hormone group withdrew after 8 weeks due to shoulder pain. Mean compliance among the rest of the subjects was 98%. The mean change in LDL cholesterol was -0.46 mmol/L (95% confidence interval CI, -1.00 to 0.09 mmol/L) in the growth hormone group versus 0.08 mmol/L (95% CI, -0.55 to 0.71 mmol/L) in the placebo group (difference not significant). No changes occurred in the levels of other lipids, lipoprotein particles, or apolipoproteins, with the exception of lipoprotein(a) Lp(a). The median changes in Lp(a) were 33% (interquartile range, 2% to 53%) and -15% (interquartile range, -22% to 18%) in the growth hormone and placebo groups, respectively (P =.02). We conclude that the effect of growth hormone on LDL cholesterol levels in FH is less than expected, based on its LDL-catabolic effects, and is counteracted by profound increases in Lp(a) levels, resulting in unchanged levels of apolipoprotein B. Thus, growth hormone is probably not useful as adjunctive therapy in FH. |
| The effect of growth hormone replacement on serum lipids, lipoproteins, apolipoproteins and cholesterol precursors in adult growth hormone deficient patients Russell-Jones, D. L., G. F. Watts, et al. (1994), Clin Endocrinol (Oxf) 41(3): 345-50. Abstract: OBJECTIVE: Adult patients with growth hormone deficiency are thought to be at higher risk of mortality from cardiovascular disease. We therefore investigated the effect of recombinant human growth hormone (rhGH) replacement therapy on fasting serum concentrations of lipids, lipoproteins and cholesterol precursors in adult growth hormone deficient patients. DESIGN: Double-blind placebo controlled trial. Patients were randomly allocated to placebo or rhGH replacement therapy (0.018 U/kg/day for 1 month followed by 0.036 U/kg/day for 1 month). PATIENTS: Eighteen patients with severe growth hormone deficiency. MEASUREMENTS: Fasting lipid, lipoprotein and cholesterol precursors (lathosterol and mevalonic acid) were measured at baseline and after 2 months. RESULTS: In the rhGH treated group there was a significant fall in serum cholesterol (P < 0.01) (6.44 +/- 0.49 to 5.71 +/- 0.48 mmol/l), LDL cholesterol (P < 0.02) (4.29 +/- 0.49 to 3.62 +/- 0.44 mmol/l), LDL cholesterol/HDL cholesterol ratio (P < 0.02) (3.99 +/- 0.62 to 3.26 +/- 0.39), apolipoprotein B (P < 0.01 (1.30 +/- 0.11 to 1.15 +/- 0.11 g/l) and mevalonic acid (P < 0.05) (13.4 +/- 10.96 to 6.21 +/- 1.91 micrograms/l). There were no significant changes in triglycerides, HDL cholesterol, apolipoprotein A1, lipoprotein (a) or lathosterol concentrations. In the GH treated group the rise in serum insulin was inversely correlated with the fall in cholesterol (P < 0.05), LDL cholesterol (P < 0.01) and apolipoprotein B (P < 0.01). There were no significant changes in any of the measured variables in the placebo group. CONCLUSION: We conclude that GH may be involved in the regulation of lipid and lipoprotein metabolism and that rhGH replacement therapy of adult GHD patients is associated with beneficial changes in lipid and lipoprotein profiles. The reduction in mevalonic acid is consistent with up-regulation of hepatic LDL receptors caused by GH and this may explain the fall in LDL cholesterol and apolipoprotein B concentrations. |
| The effect of high density lipoprotein phospholipid acyl chain composition on the efflux of cellular free cholesterol Davidson, W. S., K. L. Gillotte, et al. (1995), J Biol Chem 270(11): 5882-90. Abstract: High density lipoprotein (HDL) phospholipid (PL) fatty acyl chain composition has been proposed to affect the ability of HDL to participate in the first step of reverse cholesterol transport. To examine the effects of PL fatty acid chain length and degree of unsaturation in this process, reconstituted HDL (rHDL) particles were made with human apolipoprotein (apo) A-I and PL containing fatty acid chains from 14 to 18 carbons in length, which were either fully saturated or unsaturated in one or both chains. These particles were characterized structurally and for their ability to promote free (unesterified) cholesterol (FC) efflux from cells growing in culture. The discoidal rHDL particles were homogeneous and exhibited similar hydrodynamic diameters (10.4 +/- 1.0 nm) indicating that apoA-I forms similarly sized discs with a variety of PL. Measurements of particle surface charge, apoA-I alpha-helix content, and conformational stability indicated that the conformation of apoA-I varies among the particles. These conformational effects on apoA-I are consistent with the PL fluidity influencing the interaction between the amphipathic alpha-helical segments and PL acyl chains. Differential scanning calorimetry demonstrated that the physical state of the rHDL PL at 37 degrees C varied according to acyl chain length and degree of unsaturation; the FC efflux efficiencies for particles with PL in either the gel or liquid crystal states were determined. The ability of the rHDL to accept cellular FC depended on the physical state of the PL in the rHDL. Liquid crystal PL formed the most efficient FC acceptor particles exhibiting a maximal efflux velocity (Vmax) of 12-14% release of total cellular FC per h. Gel-phase PL formed inefficient rHDL acceptors with a Vmax of about 3%/h. A similar hierarchy of FC efflux efficiency was noted when either mouse L-cells or rat Fu5AH hepatoma cells were used as the FC donors. Furthermore, this hierarchy was found to be due to the characteristics of the PL and not due to variable apoA-I conformation because protein-free, small unilamellar vesicles made with the same PL exhibited similar relative efflux capabilities. Generally, the ability of a given rHDL particle to accept cellular FC was related to rHDL PL acyl chain length and degree of unsaturation; decreases in PL acyl chain length and increases in chain unsaturation tended to result in more efficient FC acceptor particles.(ABSTRACT TRUNCATED AT 400 WORDS) |
| The effect of high external pressure on DPPC-cholesterol multilamellar vesicles: a pressure-tuning Fourier transform infrared spectroscopy study Reis, O., R. Winter, et al. (1996), Biochim Biophys Acta 1279(1): 5-16. Abstract: We have investigated the effect of incorporation of cholesterol on the barotropic phase behavior of aqueous dispersions of 1,2-dipalmitoylphosphatidylcholine (DPPC) using Fourier-transform infrared spectroscopy (FTIR) in combination with the diamond anvil technique. Infrared spectral parameters, such as the frequencies, intensities, bandshapes and band splittings have been used to detect structural and dynamical changes upon incorporation of cholesterol into the DPPC bilayer. Analysis of these spectral parameters yields information on conformer population, reorientational fluctuations, interchain interaction, hydrogen bonding, interdigitation packing, and phase transformations of the DPPC/cholesterol mixtures. We present FTIR data of aqueous DPPC dispersions at 0, 10, 20, 30, 40, and 50 mol% cholesterol in the pressure range from 0.001 to 20 kbar at two temperatures, 25 degrees C and 55 degrees C. In addition, comprehensive temperature dependent measurements in the range from 20 degrees C to 80 degrees C were performed at ambient pressure. Analysis of the CH2 symmetric and antisymmetric stretching modes yields information of the effect of cholesterol concentration on the phase transition phenomena occurring in the lipid bilayer. Observation of the correlation field splittings of the CH2 bending and rocking modes monitors structural changes and dynamical properties of the lipid mixtures. Cholesterol induces more orientational disorder of the lipid molecules in terms of an increase of the reorientational fluctuations of the molecules and twisting/torsion motions of the acyl chains in the gel phase even at elevated pressures. It therefore appears that one important role of cholesterol is to make the membrane insensitive to changes in external environment, such as high hydrostatic pressure. Increase of pressure leads to a decrease in half width of the C = O band contour of pure DPPC and of DPPC/cholesterol mixtures, especially for cholesterol concentrations equal and higher than 30 mol%, which might be due to a marked increase in free carbonyl groups. At high pressure part of the bound water from the interfacial zone of the membrane is withdrawn. Increase of the cholesterol concentration and increase in pressure have opposite effects on the population of free and hydrated carbonyl ester groups of DPPC in the gel phases. |
| The effect of increased hepatic sitosterol on the regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and cholesterol 7 alpha-hydroxylase in the rat and sitosterolemic homozygotes Shefer, S., G. Salen, et al. (1994), Hepatology 20(1 Pt 1): 213-9. Abstract: We investigated hepatic cholesterol homeostasis in four homozygous sitosterolemic subjects from two unrelated families who showed enhanced absorption, diminished removal and increased tissue and plasma concentrations of sitosterol (24-ethyl cholesterol). Measurements of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activities were correlated with steady state messenger RNA levels and related to cholesterol 7 alpha-hydroxylase activities in the sitosterolemic homozygotes and nine controls. Similar determinations were made in rats infused intravenously with sitosterol so that hepatic and plasma sitosterol concentrations increased to about 10% of total sterols to resemble the human disease sitosterolemia. In the four sitosterolemic homozygotes, hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activities were markedly reduced (12% of normal), and steady state 3-hydroxy-3-methylglutaryl coenzyme A reductase messenger RNA levels barely detected. In contrast, hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activities and messenger RNA levels were not decreased in rats with similarly elevated hepatic sitosterol concentrations. However, hepatic cholesterol 7 alpha-hydroxylase activity was inhibited 30% in both the sitosterolemic homozygotes and rats with high liver sitosterol concentrations. Plasma cholesterol concentrations increased 120% in the sitosterol-infused rats and 29% in the untreated human homozygotes. These results demonstrate that high-tissue sitosterol concentrations do not inhibit hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activityor steady state messenger RNA levels and that they competitively block cholesterol 7 alpha-hydroxylase activity and raise plasma cholesterol levels. Thus the deficiency of 3-hydroxy-3-methylglutaryl coenzyme A reductase in the liver of sitosterolemic homozygotes is inherited and not due to the hepatic accumulation of sitosterol.(ABSTRACT TRUNCATED AT 250 WORDS) |
| The effect of interleukin 1 beta on the biosynthesis of cholesterol, phosphatidylcholine, and sphingomyelin in fibroblasts, and on their efflux from cells to lipid-free apolipoprotein A-I Kronqvist, R., P. Leppimaki, et al. (1999), Eur J Biochem 262(3): 939-46. Abstract: In this study we have investigated the effect of interleukin 1beta (IL-1beta) on the metabolism of cholesterol and choline-phospholipids in cultured fibroblasts, and also measured efflux of these lipids to lipid-free apo A-I as a function of IL-1beta treatment. Long-term exposure (up to 48 h) of cells to IL-1beta (1 ng.mL-1) markedly increased the rate of cholesterol esterification, as determined by the incorporation of 3Holeic acid into cholesteryl esters. This treatment also led to a substantially increased mass of cholesteryl esters in the cells. The accumulation of cholesteryl esters in IL-1beta-treated cells could be blocked using compound 58-035 to inhibit the activity of acyl-CoA cholesterol acyl transferase. The activation of cholesterol esterification by IL-1beta was evident within a few hours after initiation of the IL-1beta treatment. Cholesterol biosynthesis was inhibited by 25% by IL-1beta (after 48 h exposure), and this eventually led to a 20% decrease in cell cholesterol mass. Treatment of cells with IL-1beta for 48 h also reduced the synthesis of sphingomyelin and caused a 30% decrease in cell sphingomyelin mass (after 48 h at 1 ng.mL-1 of IL-1beta). IL-1beta did not stimulate an acute (within a few minutes up to an hour) degradation of cell 3Hsphingomyelin. This suggests that IL-1beta did not activate an endogenous sphingomyelinase in these cells, but only affected rates of synthesis. The rate of phosphatidylcholine synthesis was barely affected, but mass was moderately reduced by a 48-h treatment of cells with IL-1beta. Finally, the efflux of cell 3Hcholesterol, 3Hsphingomyelin, and 3Hphosphatidylcholine to lipid-free apolipoprotein A-I was markedly increased from cells treated with IL-1beta for 24 and 48 h. We conclude that long-term exposure of cells to IL-1beta had marked effects on the cellular homeostasis of cholesterol and choline-containing phospholipids. |
| The effect of Ipomoea batatas (Caiapo) on glucose metabolism and serum cholesterol in patients with type 2 diabetes: a randomized study Ludvik, B. H., K. Mahdjoobian, et al. (2002), Diabetes Care 25(1): 239-40. |
| The effect of isradipine administration on existing fatty streaks in the cholesterol-fed rabbit: a morphometric study Skepper, J. N. and C. T. Kappagoda (1996), Atherosclerosis 119(2): 247-60. Abstract: Previous studies have shown that the administration of certain calcium channel blocking drugs (at an appropriate time point) can reduce the severity of atherosclerotic lesion formation. This study was undertaken to determine if the administration of isradipine would reverse established lesions produced by feeding rabbits an atherogenic diet. Rabbits were fed cholesterol for three weeks and examined directly, or after being left for a four week washout period, with or without a daily oral supplement of isradipine. Fatty streaks were well established after three weeks of cholesterol feeding and were more extensive at the end of the washout period, as indicated by gross changes in the volume of the intima per unit length of aorta. When isradipine was administered during the washout period, the volume of the intima per unit length of aorta fell to levels below those produced by cholesterol feeding for three weeks alone. The major components of the lesions affected to accommodate these changes were the foam cells and myointimal cells; these were examined in detail using morphometry and lipid cytochemistry. The mean volume of intima/cm of aorta occupied by foam cells and myointimal cells both fell by more than 60% to levels lower than those found after three weeks of cholesterol feeding alone. The volume of the extracellular space of the intima occupied by cytochemically demonstrable unesterified and esterified cholesterol was reduced by isradipine administration as was that of foam cells, all to levels lower than those found after three weeks of cholesterol feeding alone. These data indicate that the administration of isradipine during a washout period, after cholesterol feeding, can promote the regression of fatty streak lesions. |
| The effect of ketoconazole on the cholesterol content of the blood serum lipoproteins and bile in experimental hypercholesterolemia Dushkin, M. I. and M. V. Ivanova (1992), Eksp Klin Farmakol 55(2): 47-9. Abstract: Inclusion of ketonazole (in a daily dose of 400 mg/kg for 8 days) into the diet of intact and cholesterol-fed (5% dietary cholesterol) rats produced a respective 20- and 30-percent lowering of cholesterol content in blood serum. In all the animals, the hypocholesterolemic effect of ketoconazole was realized via a decrease of the concentration of very low and low density lipoproteins. Ketoconazole also gave rise to a reduction of the concentration of cholesterol and bile acids in bile of the intact rats and of cholesterol in bile of the cholesterol-fed animals. |
| The effect of L-carnitine on cholesterol metabolism in rat (Rattus bubalus) hepatocyte cells Mondola, P., M. Santillo, et al. (1992), Int J Biochem 24(7): 1047-50. Abstract: 1. This paper concerns the study of the effect of L-carnitine on cholesterol metabolism in rat hepatocyte cells BRL-3A. In this research the binding of 125Ihuman low density lipoprotein (LDL) to BRL-3A cells and 3-hydroxy 3-methylglutaryl CoA reductase activity (HMG-CoA reductase activity) after L-carnitine incubation were studied. 2. It was found that L-carnitine is able to increase either the 125ILDL binding or inhibit the HMG-CoA reductase activity in BRL-3A cells. 3. These results indicate that L-carnitine affects the cholesterol metabolism through an inhibition of HMG-CoA reductase activity that could be responsible for the increased 125ILDL binding in rat hepatocytes. |
| The effect of linseed oil on the fatty acid composition of blood plasma low- and very low-density lipoproteins and cholesterol in diabetics Kaminskas, A., M. Levaciov, et al. (1992), Vopr Pitan(5-6): 13-4. Abstract: Twenty patients with compensated diabetes mellitus of 10-15-year duration took polyunsaturated fatty acids omega-3 (30 g of flax oil a day) in addition to their routine food. This led to an insignificant lowering in total cholesterol and elevation of cholesterol in high density lipoproteins. A significant rise in the level of omega-3 polyunsaturated fatty acids in lipoproteins occurred in 6 patients only. Minor effect of the diet oil may be due to low delta-6-desaturic activity in the majority of the examinees. The findings point to necessity to use other sources of omega-3 acids in diet therapy of diabetics, fish oil, in particular. |
| The effect of long-term antiepileptic treatment on serum cholesterol (TC, HDL, LDL) and triglyceride levels in adult epileptic patients on monotherapy Nikolaos, T., G. Stylianos, et al. (2004), Med Sci Monit 10(4): MT50-2. Abstract: BACKGROUND: Antiepileptic drugs influence, among others, cholesterol and lipoprotein serum levels. MATERIAL/METHODS: Serum cholesterol (TC, HDL-c, and LDL-c) and triglyceride (TG) levels were measured in 103 epileptic patients receiving chronic antiepileptic monotherapy and in 103 age- and sex-matched controls. RESULTS: Compared with controls, patients on carbamazepine showed significant higher TC, HDL-c, and LDL-c and non significantly higher TG values. Patients on phenobarbital showed no statistically significant differences in TC, HDL-c, LDL-c and TG values. Patients on phenytoin showed significantly higher LDL-c values and non-significant differences in TC, HDL-c and TG values. Patients on valproate showed significantly lower TC, LDL-c and TG values and non-significant differences in HDL-c values. Changes in serum lipid profiles did not correlate with drug plasma levels. CONCLUSIONS: Our results suggest a need for monitoring serum TC, HDL-c, LDL-c and TG levels and, perhaps, prescribing a low-cholesterol diet in patients receiving carbamazepine and phenytoin, but not phenobarbital. |
| The effect of long-term microcrystalline chitosan therapy on plasma lipids and glucose concentrations in subjects with increased plasma total cholesterol: a randomised placebo-controlled double-blind crossover trial in healthy men and women Metso, S., R. Ylitalo, et al. (2003), Eur J Clin Pharmacol 59(10): 741-6. Abstract: OBJECTIVE: To evaluate the long-term effect of microcrystalline chitosan (MCC) on plasma lipids, especially the concentration of low-density lipoprotein (LDL) cholesterol, in subjects with a moderately increased concentration of plasma total cholesterol. METHODS: A total of 130 middle-aged men and women without severe disease and with a total cholesterol of 4.8-6.8 mmol/l and triglycerides below 3.0 mmol/l were randomised into two treatment groups. At the beginning of the 10-month trial, all participants received placebo 1.2 g twice daily during a 1-month run-in period. Subsequently, group 1 first received 1.2 g placebo twice daily for 3 months and then 1.2 g MCC twice daily for 3 months. Correspondingly, group 2 received 1.2 g MCC twice daily during the first and 1.2 g placebo twice daily during the second 3-month period. During the final 3-month follow-up period, both groups received MCC. Altogether, 83 participants completed the study. RESULTS: No difference was detected in the change in the LDL-cholesterol concentration between the treatments during the crossover trial (P=0.98 for interaction between time period and treatment group, repeated-measures analysis of variance for crossover design). In an otherwise similar analysis, no differences were detected between the treatments in the concentrations of total cholesterol, high-density lipoprotein cholesterol, triglycerides and glucose. CONCLUSIONS: Treatment with MCC had no effect on the concentrations of plasma lipids or glucose in healthy middle-aged men and women with moderately increased plasma cholesterol concentrations. |
| The effect of long-term probucol intake on the lipoprotein cholesterol content and glutathione peroxidase activity in the blood of patients with coronary arteriosclerosis and hyperlipidemia Lankin, V. Z., V. M. Revenko, et al. (1993), Kardiologiia 33(9): 41-4, 4-5. Abstract: The authors present results of 6-month probucol (lipomal) therapy in patients with coronary heart disease concurrent with Types 2a and 2b hyperlipidemia. There were 22 and 23% increases in total cholesterol and low density lipoprotein cholesterol, respectively, whereas the levels of high density lipoprotein decreased and triglycerides remained unchanged. Having antioxidative properties, probucol enhanced the activity of the antioxidative enzyme glutathione peroxidase on an average twice, which should be borne in mind in evaluating the efficiency of treatment. |
| The effect of long-term thyroxine on bone mineral density and serum cholesterol Fowler, P. B., J. McIvor, et al. (1996), J R Coll Physicians Lond 30(6): 527-32. Abstract: The effect of thyrotrophin suppression on bone mineral density (BMD) and serum cholesterol concentration was assessed in 31 treated hypothyroid women. Measurements of the BMD of the lumbar spine and femoral neck were repeated in seven of those with the lowest value after an average period of 22.7 months. Final cholesterol concentrations were compared with values before thyroxine was started. The dose of thyroxine was based on clinical assessment, serum triiodothyronine concentrations kept within the normal range, and thyrotrophin values within the normal range or suppressed. The patients had taken thyroxine replacement for a mean of 12.7 years. Two-thirds (21 subjects) had suppressed thyrotrophin concentrations, and it was normal in one-third (10). Fifteen subjects had a past history of thyrotoxicosis. BMD and cholesterol concentrations were compared between those with suppressed and normal thyrotrophin concentrations and between those with and without a past history of thyrotoxicosis. No patient had a pathological fracture. One had a Z value for the femoral neck of -1.6, denoting early but definite osteoporosis, and five had borderline osteoporosis with Z values for one or other site between -1.1 and -1.5. None of the seven with the lowest BMDs had any significant change when measurements were repeated. The difference in Z values between subjects with suppressed and normal thyrotrophin concentrations was not significant for either the lumbar spine (p = 0.68) or the femoral neck (p = 0.28). A past history of thyrotoxicosis had a greater effect on BMD for both sites than thyrotrophin suppression, but again the difference between those with and without a past history of thyrotoxicosis was significant neither for the lumbar spine (p = 0.18) nor for the femoral neck (p = 0.34). The combination of thyrotrophin suppression and a past history of thyrotoxicosis also failed significantly to reduce the BMD of the lumbar spine (p = 0.38) or femoral neck (p = 0.30) in comparison with those who had neither thyrotrophin suppression nor a past history of thyrotoxicosis. The mean fall in serum cholesterol concentration was 2.1 mmol/l (SD 1.78) (p = 0.001) in those with a suppressed thyrotrophin concentration taking a mean daily dose of thyroxine of 171 micrograms (SD: 34.7), compared with a fall of 0.89 mmol/l (SD: 1.04) (p = 0.065) in those whose thyrotrophin concentration was not suppressed on a mean daily thyroxine dose of 140 micrograms (SD: 50). No patient had atrial fibrillation or cardiographic evidence of coronary artery disease (CAD). The serum cholesterol concentration should play at least as important a part in influencing the dose of thyroxine as a fear of osteoporosis. Fractures are not a feature in the natural history of treated hypothyroidism, whereas CAD is a common cause of death in these patients. |