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PubMed1995

Expression and distribution of cholesterol 7 alpha-hydroxylase in rat liver.

The hydroxylation of cholesterol by cholesterol 7 alpha-hydroxylase (CYP7) to 7 alpha-hydroxycholesterol is the rate-limiting step in the production of bile acids. An anti-peptide antibody targeted to the C-terminus of CYP7 was produced by immunising rabbits with the synthetic peptide Tyr-Lys-Leu-Lys-His. The antibody bound to a single band of 54 kDa from rat hepatic microsomal fractions. The intensity of the band was subject to a diurnal variation and showed a significant increase (P < 0.01) in apoprotein at night. Treatment of rats with cholestyramine increased CYP7 apoprotein in the morning (P < 0.005) and at night (P < 0.005), but diurnal variation was maintained. CYP7 catalytic activity, measured using a specific gas chromatography/mass spectrometry assay, showed similar changes in the pattern of diurnal variation and induction. The distribution of CYP7 in rat liver tissue sections was investigated by immunocytochemistry. In sections from rats treated with cholestyramine, there was an even distribution of immunoreactivity, except in the proximal perivenous hepatocytes where immunoreactivity was slightly more intense. A similar distribution was found in sections from untreated rat liver, except immunoreactivity was overall slightly less intense. This study shows that the C-terminus of CYP7 is a useful epitope for the targeting of anti-peptide antibodies.

Acetates↗

PubMed1991

Low density lipoprotein receptor levels and the response to dietary and pharmacological intervention in polygenic hypercholesterolemia.

To assess its hypolipidemic predictive value, maximally induced low density lipoprotein receptor activity was measured in vitro in peripheral blood lymphocytes from 20 polygenic hypercholesterolemic patients prior to their recruitment into a rigorous dietary and pharmacological treatment program. The patients in the diet program demonstrated significant beneficial changes in plasma, LDL and HDL cholesterol concentrations. After 12 weeks, those patients who had not had reductions in LDL cholesterol to within the reference range, had cholestyramine and/or bezafibrate supplements to the diet for a further six weeks. The beneficial trends continued. The LDL receptor values correlated well with pre-treatment LDL cholesterol and plasma apoprotein B concentrations (r = -0.472, P less than 0.01 and r = -0.526, P less than 0.01, respectively) and with the percentage change induced by diet (r = 0.510, P less than 0.01 and r = 0.480, P less than 0.01, respectively) and by diet supplemented with bezafibrate and cholestyramine (r = 0.634, P less than 0.05 and r = 0.629, P less than 0.05, respectively). In polygenic hypercholesterolemic patients in whom LDL receptor activity is high, treatment with diet alone may be sufficient whereas those with low receptor activity would require specific pharmacological intervention.

Adult↗

PubMed1991

The plasma level of 7 alpha-hydroxy-4-cholesten-3-one reflects the activity of hepatic cholesterol 7 alpha-hydroxylase in man.

Circulating levels of 7 alpha-hydroxy-4-cholesten-3-one have been compared with activities of the rate-limiting enzyme in bile acid synthesis, microsomal cholesterol 7 alpha-hydroxylase, measured in liver biopsies obtained from patients undergoing surgery for gallstone disease. Some patients were treated with cholestyramine or bile acids prior to operation in order to alter the feed-back inhibition of the enzyme. The levels of the sterol were similar in untreated patients and in patients treated with ursodeoxycholic acid (median concentration 17 and 13 ng/ml, respectively), and so were the activities of the enzyme (median activity 7.0 and 5.5 pmol/min/mg protein, respectively). The sterol levels and enzyme activities were significantly increased in patients treated with cholestyramine (91 ng/ml and 45 pmol/min/mg protein) and decreased in patients treated with chenodeoxycholic acid (less than 2.0 ng/ml and 0.7 pmol/min/mg protein). There was a strong positive correlation (r = 0.90, P less than 0.00001) between levels of 7 alpha-hydroxy-4-cholesten-3-one in plasma and the activities of cholesterol 7 alpha-hydroxylase in the whole patient group. The results show that analysis of 7 alpha-hydroxy-4-cholesten-3-one in plasma is a sensitive and convenient method to determine relative rates of bile acid production in man.

Adult↗

PubMed1989

Bile acid synthesis in humans: regulation of hepatic microsomal cholesterol 7 alpha-hydroxylase activity.

The present work tested the hypothesis that portal venous bile acids regulate the activity of the cholesterol 7 alpha-hydroxylase and studied the influence of hepatic microsomal free cholesterol concentration on the enzyme activity. Operative liver biopsies and samples of portal venous blood were obtained from a total of 61 patients with gallstones who were undergoing cholecystectomy. Fifteen of the patients were treated with cholestyramine (16 g/day) for 2-3 wk before operation and 23 patients with chenodeoxycholic acid (15 mg/kg.day) or ursodeoxycholic acid (15 mg/kg.day) for 3-4 wk before operation. Highly accurate methods based on isotope dilution-mass spectrometry were used for assay of the cholesterol 7 alpha-hydroxylase activity, the concentration of free cholesterol in the microsomes, and the levels of individual bile acids in portal venous blood. Cholestyramine treatment increased the cholesterol 7 alpha-hydroxylase activity about sixfold, from 7.6 +/- 1.1 (mean +/- SEM) to 45.7 +/- 6.7 pmol/min.mg protein. Administration of chenodeoxycholic acid reduced the enzyme activity considerably to 1.0 +/- 0.3 pmol/min.mg protein, whereas ursodeoxycholic acid did not significantly affect the enzyme activity (7.9 +/- 2.2 pmol/min.mg protein). The concentration of microsomal free cholesterol remained essentially unchanged in spite of a 45-fold variation in enzyme activity. There was a negative correlation between the absolute as well as the relative concentration of chenodeoxycholic acid in portal blood and the activity of the cholesterol 7 alpha-hydroxylase, whereas there was no correlation between the total concentration of bile acids and the enzyme activity. It is concluded that the composition of individual bile acids may be more important than the total concentration of bile acids in the portal vein for the regulation of the cholesterol 7 alpha-hydroxylase activity in humans. It is further concluded that chenodeoxycholic acid is a considerably stronger suppressor of bile acid synthesis than ursodeoxycholic acid.

Adult↗

PubMed1978

Treatment of established atherosclerosis during cholesterol feeding in monkeys.

A semipurified diet containing 43% of the calories as fat and 1.2 mg of cholesterol/cal was fed to cynomolgus monkeys (Macaca fascicularis) for 6 months; the cholesterol content was reduced to 0.34 mg/cal for the next 18 months. During the latter period, the monkeys were assigned to 4 groups of 18 animals each and received the following dietary additions: A, none (controls); B, cholestyramine (5%, w/w); C, dextrothyroxine (0.003%); and D, Wy-14,643 (0.45%). Cholestyramine normalized plasma lipid levels and reduced the size of aortic and coronary atherosclerotic lesions in spite of the high-fat, high-cholesterol intake. Dextrothyroxine reduced cholesterolemia but did not modify the extent of arterial lesions. Wy-14,643 changed neither plasma cholesterol levels nor the extent of atherosclerosis.

Acetates↗

PubMed1982

The metabolism of very low density and intermediate density lipoproteins in patients with familial hypercholesterolaemia.

The metabolism of apolipoprotein B (apoB) in very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) was studied in normal subjects and in patients with familial hypercholesterolaemia (FH) after an intravenous injection of autologous VLDL labelled with 125I. There were no significant differences in half life, pool size and turnover rate (mg/kg/h) of VLDL-apoB between the normal subjects, the FH heterozygotes and the FH homozygotes. IDL-apoB metabolism in the FH patients differed significantly from that in the normal subjects. In the FH patients, the rise to the maximum of the specific activity curve was slower, the half life of the descending limb of the specific-activity curve was longer, the fractional rate of turnover was lower and the plasma concentration was higher than in the normals. The effect of cholestyramine on IDL-apoB metabolism in the normal subjects did not differ from that in the FH heterozygotes and homozygotes, though cholestyramine is known to stimulate hepatic uptake of low density lipoprotein (LDL) by the LDL receptor. It is suggested that in normal human subjects the LDL receptor makes some contribution to the hepatic uptake of IDL-apoB derived from VLDL, but that IDL uptake is mediated partly by a separate receptor that recognizes apolipoprotein E but not apoB.

Adolescent↗

PubMed1985

Effect of plasma exchange with and without concomitant drug treatment on lipids and lipoproteins in patients with familial hypercholesterolemia confirmed by tissue culture.

Repeated plasma exchange is an effective treatment for young patients with familial hypercholesterolemia. We treated 2 homozygous and 1 heterozygous patient with very high cholesterol levels with continuous plasma exchange using human albumin solution as exchange medium. The treatment was repeated every 2 weeks in 2 patients and weekly in the third. Treatment periods of plasma exchange alone and of plasma exchange with concomitant drug therapy were compared. For drug treatment beta-pyridylcarbinol, the alcohol corresponding to nicotinic acid (0.9 g/day equivalent to 3 g of nicotinic acid) and cholestyramine (16 g/day) were used. Plasma exchange alone resulted in a decrease of all lipids by 55% and of apolipoproteins by 50-60% as compared to the plasma levels before exchange. Subsequently all lipoproteins rose again to reach pre-exchange levels within about 2 weeks. There was no difference between the homozygous and the heterozygous patients. Beta-pyridylcarbinol or cholestyramine given concomitantly did not alter the post-exchange increase of total, LDL, HDL cholesterol nor of the corresponding apolipoproteins except of apolipoprotein B.

Adult↗

PubMed1990

Effect of probucol treatment on the susceptibility of low density lipoprotein isolated from hypercholesterolemic patients to become oxidatively modified in vitro.

Lipid accumulation in monocyte-originated macrophages in the subendothelial space is an important characteristic of atherosclerotic lesions. Several lines of evidence have indicated that this accumulation occurs as a result of lipid peroxidation. In the present study the ability of probucol to prevent oxidation of low density lipoprotein (LDL) was investigated in 20 hypercholesterolemic individuals taking part in the Probucol Quantitative Regression Swedish Trial (PQRST). The effect of Cu2(+)-induced oxidation of LDL on degradation by macrophages, binding to LDL receptors on fibroblasts and LDL TBARS content was analysed. With LDL isolated from patients on diet alone oxidation led to a 44.3% decreased binding to fibroblasts (P less than 0.001), a ninefold increased uptake in macrophages (P less than 0.001) and a twentyfold increase in TBARS content (P less than 0.001) as compared to native LDL. These values were essentially the same during treatment with cholestyramine alone. However, during treatment with probucol plus cholestyramine exposure of LDL to Cu2+ resulted in an increase in TBARS which was less than 50% (P less than 0.02) of that observed during the other two treatment periods. Furthermore, probucol treatment abolished more than 70% of the decrease in B,E receptor binding to fibroblasts (P less than 0.05) and more than 90% of the increased degradation by macrophages (P less than 0.001) of Cu2+ oxidatively modified LDL.

Aged↗

PubMed1991

Long-term efficacy and safety of simvastatin alone and in combination therapy in treatment of hypercholesterolaemia.

The 3-years efficacy and safety of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin (S) (previously called synvinolin or MK-733) has been studied in single and combined therapy with cholestyramine (C) in 48 hypercholesterolaemic patients. Plasma lipids, lipoproteins and apolipoproteins A-I and B, and blood safety tests (haematology, liver function, creatine phosphokinase (CPK), creatinine, blood glucose and thyroid function) were determined regularly throughout the study. Extensive ophthalmological examinations with particular focus on the lens were done before initiation of therapy and at every 6 months during drug treatment. Maximal reductions of mean plasma total cholesterol concentration (34% with S; 47% with S + C) and low-density lipoprotein (LDL)-cholesterol concentration (42% with S; 56% with S + C) were achieved after 4 weeks on full-dose therapy. During continued treatment, years 1 through 3, the reduction of mean plasma total cholesterol was 26-29% with S alone, and 31-41% with S + C. Significant reductions of plasma triglycerides (15-27%) and very low density lipoprotein (VLDL) triglycerides (10-27%) were achieved in the group treated with S as single therapy. In this group there was also a significant increase (10-14%) of high-density lipoprotein (HDL)-cholesterol. In liver aspartate (AST) and alanine (ALT) aminotransferases, as well as alkaline phosphatase (ALP), minor and variable, but usually transient, increases were seen. Repeated ophthalmological examinations did not demonstrate any drug-related side effects. It is concluded that simvastatin is a safe and efficient cholesterol-lowering drug for long-term therapy, both as a single drug and in combination with cholestyramine.

Adult↗

PubMed1989

Bile salt binding by maalox, sucralfate, and meciadanol: in vitro and clinical comparisons.

Inhibition of gastric acid secretion is a major factor in protecting the gastric mucosa, although other mechanisms such as bile salt binding may contribute to the protective properties of individual agents. Sucralfate, antacid (Maalox), and Meciadanol, a new flavonoid, were compared with cholestyramine resin for binding bile salts. The free, glycine, and taurine conjugates of the human bile salts, cholate, chenodeoxycholate, and deoxycholate, were incubated with each of the above. Cholestyramine resin adsorbed 91-97% of all bile salts tested. Meciadanol adsorbed all of the bile salts fairly well except for the free forms of chenodeoxycholate and deoxycholate. Meciadanol (53 to 84%) adsorbed bile salts better than sucralfate (4.2 to 61%), and significantly (P less than 0.05) better than Maalox (10 to 47%). In our in vitro studies, sucralfate was not as effective in binding bile salts as previously reported. Patients in the surgical intensive care unit were randomized prospectively to receive nasogastric instillation of Maalox, sucralfate, or Meciadanol to prevent gastrointestinal bleeding. The gastric aspirates were analyzed for bile salt concentration. The mean bile salt concentration of those treated with Maalox (0.24 mM), Meciadanol (0.24 mM), or sucralfate (0.35 mM) was significantly lower than those treated with nasogastric aspiration (0.87 mM) alone (P less than 0.01). This suggests that these substances bind bile salts and may provide additional protection to the gastric mucosa along with their ability to neutralize gastric acid.

Adsorption↗

PubMed1976

Therapeutic failure in familial type II hyperlipoproteinemia.

The extended use of diet and cholestyramine therapy in familial type II hyperlipoproteinemia was examined in patients who previously participated in a short-term, double-blind trial. A striking secondary failure in therapeutic response during 4 yr of use of this therapy was noted with plasma cholesterol rising an average of 15%. A 3 mo, out-patient, follow-up study designed to reinforce patient motivation and dietary and drug adherence resulted in a prompt but partial reversal of this therapeutic deterioration in 16 patients. Additional inpatient studies confirmed that patient noncompliance with the dietary regimen was the major factor responsible for the secondary failure. Cholestyramine together with a low cholesterol diet can be an effective agent in familial type II hyperlipoproteinemia, given a comprehensive program of out-patient follow-up with continued emphasis on dietary principles and drug adherence.

Adult↗

PubMed1995

Serum retinol levels throughout 2 years of cholesterol-lowering therapy.

Some studies have reported an inverse correlation between serum cholesterol level and risk of cancer. This correlation might be due to a decrease in serum retinol, a lipid-soluble vitamin that controls cell proliferation and differentiation. We evaluated the influence of cholesterol-lowering therapy on serum retinol in 102 subjects (mean +/- SE: aged 47.1 +/- 4.1 years; body mass index, 23.8 +/- 0.6 kg/m2) with primary hypercholesterolemia treated for 2 years with different therapeutic protocols. Twenty-two subjects had been treated with diet alone, 35 with diet and fibrates, 37 with diet and hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase inhibitors (statins), and eight with diet and cholestyramine. Postabsorptive serum retinol, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride levels were determined at baseline and every 3 months. Baseline TC and LDL-C were significantly lower in the diet-treated group than in other groups. No intergroup differences were found in pretreatment levels of triglycerides and serum retinol. After 2 years of treatment, TC and LDL-C serum levels were not significantly decreased in the diet-alone group, whereas they were decreased by 20% and 24%, respectively, in the gemfibrozil group, 28% and 34% in the statins group; and 21% and 27% in the cholestyramine group. In the entire population (N = 102), serum retinol was 3.46 +/- 0.08 mumol/L before therapy and 3.76 +/- 0.07 after 2 years of therapy (P < .001). Serum retinol increased in diet- and statin-treated groups, but not in fibrate- and resin-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effect of estradiol and progesterone on cholesterol 7 alpha-hydroxylase activity in rats subjected to different feeding conditions.

The regulation of cholesterol 7 alpha-hydroxylase activity by estradiol and progesterone was investigated in liver microsomes isolated from rats fed standard diet, either ad libitum or fasted for 24 h, and diet containing the bile acid sequesterant cholestyramine. Differential effects were observed when the direct action of estradiol and progesterone on microsome preparations was examined. Cholesterol 7 alpha-hydroxylase activity was inhibited by progesterone in a dose-dependent way to almost complete abolition; similar patterns of declines were found in the three feeding groups under study. In contrast, the addition of 5 microM estradiol induced small and selective 7 alpha-hydroxylase increases in fasting and cholestryamine-fed animals, then activity declined to control values and consistent decreases were found from 20 microM. The administration of estradiol (50 micrograms) or progesterone (100 micrograms) for 21 days resulted in depressed cholesterol 7 alpha-hydroxylase activity in rats with high bile acid synthesis basal rate due to cholestyramine feeding. In rats receiving a standard diet, either ad libitum or after 24 h fasting, the hormonal effects did not reach significance. Declines in the content of free cholesterol were provoked by progesterone, not by estradiol, in liver microsomes prepared from all feeding groups. No changes in cholesterol 7 alpha-hydroxylase activity and microsomal free cholesterol were observed after administration of the sex hormones for 3 days. Rapid and transient inhibitions in 7 alpha-hydroxylase activity were found after the single injection of progesterone to fed animals. Estradiol, on the contrary, was unable to alter rapidly the hepatic 7 alpha-hydroxylase capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

National Heart, Lung, and Blood Institute type II Coronary Intervention Study: design, methods, and baseline characteristics.

The Type II Coronary Intervention Study (Type II Study) is a double-blind, randomized, placebo-controlled clinical trial conducted by the Division of Intramural Research of the National Heart, Lung, and Blood Institute of Bethesda, Maryland. The study was designed to evaluate the 5-year treatment effect of cholestyramine on low density lipoprotein (LDL) cholesterol and on lesions in the coronary arteries. One hundred forty-three patients with Type II hyperlipoproteinemia (elevated LDL cholesterol) and coronary artery disease (CAD) were entered into the study between 1972 and 1976. Patients were stratified by sex and extent of coronary disease as defined angiographically and were randomly allocated to a daily dosage of 24 g cholestyramine and diet (treatment group) or placebo and diet (control group). Changes in the coronary arteries were evaluated by sequential coronary angiography carried out before and after five years of treatment. This report describes the trial design and baseline characteristics of the study patients.

Adult↗

PubMed1975

Effect of 17alpha-ethinylestradiol on biliary excretion of bile acids.

The effect of 17alpha-ethinylestradiol on biliary bile acids has been investigated. The ratio of cholate to chenodeoxycholate was diminished by the estrogen in cholestyramine-treated rats. With low doses, this effect was due to increased excretion of chenodeoxycholate. With the highest dose, the decreased ratio was due to a reduction in the levels of cholic acid. In the intermediate dosage range, both factors contributed to the decreased ratio. Prolonged treatment with 500 mug daily of 17alpha-ethinylestradiol produced a reduction in the excretory rate of both bile acids in animals treated or not treated with cholestyramine.

Animals↗

PubMed2005

Designing of the centers for adsorption of bile acids on a silica surface.

Silicas chemically modified with attached aminopropyl, imidazolyl, and trimethylsilyl groups, with adsorptive and coordinative grafted hemin were synthesized. Adsorption of some bile acids on the surface of hydroxylated silica, synthesized siliceous adsorbents and cholestyramine has been studied. It was found that the main contribution to the total adsorption is caused by electrostatic attraction between anions of bile acids and positively charged sites of the surface of modified silica and also by dispersion interactions between steroid skeleton of bile acids and functional groups of modified silicon dioxides. It was established that the kinetic parameters of adsorption and adsorptive capacity for all investigated siliceous adsorbents exceed similar characteristics for cholestyramine. The best of synthesized adsorbents is hemin-containing adsorbent IX, and the sequence of increase in its adsorptive capacity in relation to bile acids corresponds to the following series: I < III < II, IV < VI < V < VIII < VII < IX.

Adsorption↗

PubMed1995

Efficacy of fluvastatin, a totally synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. FLUENT Study Group. Fluvastatin Long-Term Extension Trial.

The Fluvastatin Long-Term Extension Trial (FLUENT) was designed to assess the safety and efficacy of fluvastatin over a prolonged period of time. In this way, FLUENT represents a clinical scenario that is closer to office-based chronic treatment of hyperlipidemic patients. A total of 918 patients with severe primary hypercholesterolemia (mean baseline low density lipoprotein cholesterol [LDL-C], 227 mg/dL) were enrolled into the study and received open-label fluvastatin, 20 or 40 mg daily, depending on response. Results of the first year of treatment have been published previously and showed statistically significant changes in LDL-C (-30.7%), total cholesterol (-21.9%), and high density lipoprotein cholesterol (HDL-C; +3.5%). Of the original number of patients completing the 1-year study, 761 completed a second year of evaluation; the results are presented here. Any patient who did not achieve LDL-C levels of < or = 130 mg/dL could receive cholestyramine (usually 8 g/day) or fluvastatin up to 80 mg/day. At the end of the 2-year period there were significant changes in LDL-C with fluvastatin (20 mg/day, -25.4%; 40 mg/day, -30.6%; 80 mg/day, -33.7%; p < 0.001 vs baseline for all values). The combination of fluvastatin and cholestyramine changed LDL-C by -34.6%. Similar dose-response results were seen with reductions in total cholesterol and the LDL-C: HDL-C ratio. There were no unexpected or severe adverse events or laboratory abnormalities. In conclusion, fluvastatin offers a range of LDL-C reduction (25-34%) similar to other HMG-CoA reductase inhibitors, that conforms with guideline recommendations for over 90% of hypercholesterolemic patients.

Adult↗

PubMed1995

Fluvastatin in severe hypercholesterolemia: analysis of a clinical trial database.

Many patients with severe primary hypercholesterolemia--low density lipoprotein cholesterol (LDL-C) > 240 mg/dL--have heterozygous familial hypercholesterolemia. In such familial hypercholesterolemic patients, the lipid-lowering efficacy of fluvastatin is related to genetic factors, and it is of interest whether the response to treatment differs from that in patients with more moderate hypercholesterolemia. Thus an exploratory analysis of randomized, controlled clinical trials and their open-label extensions (12-78 weeks), conducted worldwide with fluvastatin > or = 20 mg/day (n = 1810) and placebo (n = 783), assessed whether, apart from the potential differences between familial hypercholesterolemic and nonfamilial hypercholesterolemic patients, the response to 40 mg of fluvastatin is influenced by baseline plasma lipid levels in relation to disease severity. Entry criteria included LDL-C > or = 190 mg/dL with < or = 1 risk factor and no coronary artery disease, or > or = 160 mg/dL with > 1 risk factor or definite coronary artery disease. Of these patients, 591 (33%) given fluvastatin (20-40 mg/day) and 187 (24%) given placebo had severe hypercholesterolemia with baseline LDL-C > 240 mg/dL. In controlled studies, the mean +/- SD duration of exposure was 21.1 +/- 16.1 and 19.4 +/- 15.5 weeks for fluvastatin and placebo, respectively, whereas long-term efficacy was assessed after 55.3 +/- 21.7 weeks (fluvastatin) and 21.1 +/- 12.3 weeks (fluvastatin + cholestyramine, after previous monotherapy). In summary, fluvastatin at 40 mg/day lowered LDL-C by 25-26% from baseline in controlled studies (n = 622), and by 27% in long-term studies (32-33% with fluvastatin + cholestyramine; n = 386), irrespective of severity of cholesterolemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗