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PubMed1999

Effects of dietary phytosterols on cholesterol metabolism and atherosclerosis: clinical and experimental evidence.

Although plant sterols (phytosterols) and cholesterol have similar chemical structures, they differ markedly in their synthesis, intestinal absorption, and metabolic fate. Phytosterols inhibit intestinal cholesterol absorption, thereby lowering plasma total and low-density lipoprotein (LDL) cholesterol levels. In 16 recently published human studies that used phytosterols to reduce plasma cholesterol levels in a total of 590 subjects, phytosterol therapy was accompanied by an average 10% reduction in total cholesterol and 13% reduction in LDL cholesterol levels. Phytosterols may also affect other aspects of cholesterol metabolism that contribute to their antiatherogenic properties, and may interfere with steroid hormone synthesis. The clinical and biochemical features of hereditary sitosterolemia, as well as its treatment, are reviewed, and the effects of cholestyramine treatment in 12 sitosterolemic subjects are summarized. Finally, new ideas for future research into the role of phytosterols in health and disease are discussed.

Anticholesteremic Agents↗

PubMed1982

A prospective study of 18 patients with cholestasis of pregnancy.

In this prospective study we evaluate the role of serum bile acids in the investigation and management of cholestasis of pregnancy in a detailed study of 18 patients. Bile acids were the most sensitive diagnostic test. The increased incidence of fetal distress (33.3% in this series) and meconium-stained fluid (58.3%) did not correlate with very high values of bile acids in maternal serum, umbilical cord serum, or amniotic fluid. Treatment of pruritus with cholestyramine and/or phenobarbital is ineffective in this condition, induction of labor is suggested once fetal lung maturity is established.

Adolescent↗

PubMed1997

Reduced cholesterol absorption in hamsters by crilvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.

Crilvastatin, a new drug from the pyrrolidone family, has been previously shown to inhibit the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, in vitro and in vivo, to reduce the absorption of dietary cholesterol and to stimulate the activity of cholesterol 7 alpha-hydroxylase in the rat. The aim of this study was to evaluate the effects of crilvastatin on cholesterol and bile acid metabolism in the hamster. In hamsters fed on a lithogenic diet for 8 weeks, crilvastatin treatment (200 mg/day per kg body weight) did not change plasma lipid levels, failed to improve bile parameters and did not prevent gallstone formation. In hamsters fed on a basal cholesterol-rich (0.2%) diet for 8 weeks, crilvastatin at the same dose reduced the cholesterol level in the plasma by 20%, with a decrease of both low-density and high-density lipoprotein cholesterol. The drug did not significantly stimulate the biliary secretion of bile acids but significantly decreased the activity of acyl coenzyme A:cholesterol acyltransferase in the small intestine by 64%. This effect was enhanced when cholestyramine, a bile acid-sequestering resin, was given in combination with crilvastatin. Crilvastatin alone did not change the activity of cholesterol 7 alpha-hydroxylase in the liver, despite the marked reduction in both hepatic cholesterogenesis and intestinal absorption of dietary cholesterol (the absorption coefficient was 44 +/- 2% in treated hamsters vs. 61 +/- 7% in controls).

Animals↗

PubMed2000

cDNA-derived amino acid sequence of acetoacetyl-CoA synthetase from rat liver.

In order to examine the primary structure of acetoacetyl-CoA synthetase (acetoacetate-CoA ligase, EC 6.2.1.16; AA-CoA synthetase), the cDNA clone encoding this enzyme has been isolated from the cDNA library which was prepared from the liver of rat fed a diet supplemented with 4% cholestyramine and 0.4% pravastatin for 4 days. Nucleotide sequence analysis of cloned cDNA revealed that AA-CoA synthetase of rat liver contains an open reading frame of 2019 nucleotides, and the deduced amino acid sequence (672 amino acid residues) bears 25.0 and 38.9% homologies with acetyl-CoA synthetases of Saccharomyces cerevisiae and Archaeoglobus fulgidus, respectively.

Amino Acid Sequence↗

PubMed1998

Effect of bile acid composition and manipulation of enterohepatic circulation on leptin gene regulation.

In the rat, the ob gene product, leptin, putatively regulates energy balance via appetite control and energy expenditure. Bile acids in the intestinal lumen are necessary for efficient absorption of dietary lipids and may trigger the release of regulatory peptides. To investigate whether bile acids play a role in leptin gene expression, we altered the bile acid pool and then measured leptin mRNA levels in adipose tissue. Rats fed cholic acid (1% of chow wt/wt) for 2 weeks did not gain weight as rapidly as pair-fed control animals. Despite the lower weight, normalized leptin mRNA levels were 24% greater in cholic acid-fed rats compared with controls. Conversely, cholestyramine, a bile acid sequestrant, in chow (5% wt/wt) resulted in a 26% decline in leptin mRNA. Ligation of the common bile duct or chronic biliary diversion, experimental manipulations that decreased the intestinal concentration of bile salts, decreased leptin gene expression by 30% and 50%, respectively. A fluid and electrolyte (F/E) solution with and without taurocholate (36 micromol/h x 100 g rat[-1]) was then infused for 12 hours into the duodenum in animals with chronic biliary diversion. Taurocholate infusion resulted in a fourfold increase in steady-state adipocyte leptin mRNA levels compared with F/E infusion. Intravenous infusion of taurocholate or incubation of cultured adipocytes with taurocholate had no effect on leptin mRNA levels. We conclude that bile acids upregulate leptin gene expression indirectly, probably via effects on the absorption of dietary lipids or the release of neurohumoral mediators.

Adipocytes↗

PubMed1998

The hypocholesterolemic and antiatherogenic effects of Cholazol H, a chemically functionalized insoluble fiber with bile acid sequestrant properties in hamsters.

Cholazol H (Alpha-Beta Technology, Worcester, MA), a chemically functionalized, insoluble dietary fiber with bile acid sequestrant properties, was studied in 30 male F1 B Golden Syrian hamsters for its effect on plasma lipid concentrations and early atherogenesis in experiment 1. In experiment 2, 30 male Golden Syrian hamsters were studied for the effects on plasma lipids and fecal excretion of bile acids. In experiment 1, three groups of 10 hamsters each were fed a chow-based hypercholesterolemic diet supplemented with 5% coconut oil and 0.1% cholesterol for 6 weeks. After 6 weeks, hamsters were continued on the diet with either 0% drug (hypercholesterolemic diet [HCD]), 0.5% cholestyramine (CSTY), or 0.5% Cholazol H for 8 weeks. Fasting plasma lipids were measured at weeks 6, 10, and 14, and early atherosclerosis (fatty streak formation) was measured at week 14. Relative to HCD, CSTY and Cholazol H significantly lowered plasma total cholesterol (TC) (-37%, P < .03, and -30%, P < .04, respectively) and plasma very-low and low-density lipoprotein-cholesterol (nonHDL-C) (-45%, P < .02, and -36%, P < .03, respectively) with no significant effects on plasma HDL-C or triglycerides (TG). Despite similar reductions in nonHDL-C, only Cholazol H significantly prevented early atherosclerosis (-38%, P < .02) relative to HCD. In experiment 2, three groups of 10 hamsters each were fed a chow-based hypercholesterolemic diet supplemented with 10% coconut oil and 0.05% cholesterol and either 0% drug HCD, 0.5% CSTY, or 0.5% Cholazol H for 4 weeks. Fasting plasma lipids were measured at weeks 2 and 4, and fecal bile acids were measured at week 4. Both Cholazol H and CSTY were equally effective in significantly lowering plasma TC (-16%, P < .003, and -13%, P < .01, respectively) and nonHDL-C (-22%, P < .004, and -18%, P < .02, respectively), with no significant effect on HDL-C and TG relative to HCD. Cholazol H and CSTY produced a significantly greater concentration of fecal total bile acids (39%, P < .001, and 28%, P < .002, respectively) relative to HCD. Also, there was a 48% (P < .002) and 65% (P < .001) greater fecal concentration of cholic acid (CA) for Cholazol H-treated hamsters compared with HCD- and CSTY-treated hamsters, respectively. Cholazol H also significantly increased fecal concentration of deoxycholic acid (DCA; 56%, P < .02) compared with HCD. In summary, Cholazol H is as effective as CSTY for prevention of diet-induced hypercholesterolemia and early atherosclerosis in hamsters.

Animals↗

PubMed1978

The suppressive effect of the catatoxic steroid, pregnenolone-16alpha-carbonitrile, on liver microsomal cholesterol-7alpha-hydroxlyase.

The effect of the catatoxic steroid, 3beta-hydroxy-20-oxo-5-pregnene-16alpha-carbonitrile [pregnenolone-16alpha-carbonitrile (PCN)] on hepatic microsomal cholesterol-7alpha-hydroxylase, the probable rate-limiting enzyme of bile acide biosynthesis, has been studied. Short term administration (3 days) of PCN in the diet of rats resulted in a significant decrease in the liver microsomal cholesterol-7alpha-hydroxylase activity, in contrast to a marked stimulation of microsomal cytochrome P-450 and ethylmorphine demethylase activity. PCN significantly depressed the cholesterol-7alpha-hydroxylase activity in the livers of rats with elevated levels of the enzyme produced by cholestyramine feeding. The results indicate the presence of separate control mechanisms in the regualtion of bile acid synthesis and drug metabolism.

Animals↗

PubMed1981

Effect of estrogens on beta-hydroxy-beta-methylglutaryl coenzyme A reductase activity and cholesterol levels.

The effect of estrogens on hepatic beta-hydroxy-beta-methylglutaryl coenzyme A reductase activity and cholesterol in serum and liver of ovariectomized rats on normal diet 2% cholestyramine diet or 2% cholesterol diet was investigated. Estrogen administration to ovariectomized rats on normal diet resulted in increased reductase activity and was correlated with decreased serum cholesterol and increased liver cholesterol levels with mestranol (ME), ethinyl estradiol (EE) and estradiol benzoate (EB, 250 microgram) but increased serum and liver cholesterol levels with 25 microgram and 100 microgram EB administration. The increased stimulation of reductase activity by estrogen administration was abolished when rats were fed a 2% cholesterol diet. Cholestryramine feeding markedly increased reductase activity in livers of ovariectomized rats. These studies show that estrogens are not absolutely required for the stimulation of reductase activity and therefore is consistent with the model in which cholesterol functions as a feedback repressor of reductase activity.

Animals↗

PubMed1976

Postoperative alkaline reflux gastritis.

1. The syndrome of reflux gastritis is produced by the actions of bile and upper intestinal and pancreatic secretions alone or in combination on an altered gastric mucosa. 2. The triad of epigastric pain unrelieved by antacids, bilious vomiting, and weight loss, particularly after a gastric operation should make one suspect this syndrome. Anemia due to loss of blood and dysphagia occur less frequently. 3. The definitive diagnosis is made by endoscopy. Barium studies are of less value. Acid secretory studies are not diagnostic and are of academic interest. 4. Medical treatment utilizes antacids and cholestyramine alone or together. Good, long-lasting results with these are infrequent. Despite these results, medical treatment should be tried first. 5. Surgical treatment consists of diversion of the biliary and upper intestinal secretions from the stomach and doing a vagotomy with or without a distal gastric resection to prevent a marginal ulcer from developing. 6. The two most popular operations are a Roux-en-Y diversion or interposed peristaltic jejunal limb. The simplicity of the former has made this more popular with most American surgeons. 7. The results of surgery are good to excellent in 75 to 95 per cent of cases. Relief of symptoms, improvement in histologic and secretory studies, and weight gain should be anticipated. 8. Less than optimal results are reported when the surgical diversion has not been total, gastric stasis persists, or other postgastrectomy sequelae accompany reflux gastritis.

Cholestyramine Resin↗

PubMed1982

Increased leucocyte oxidative metabolism in hyperlipoproteinaemia.

Polymorphonuclear leucocytes (PMN) from a group of subjects with hyperlipoproteinaemia (HLP) had higher oxidative metabolism with greater release of superoxide anion (O2-) than PMN from age-matched controls. Release of O2- was significantly correlated with serum cholesterol and light-density-lipoprotein-cholesterol levels, PMN from HLP subjects also has higher hexose monophosphate shunt activity and chemiluminescence than controls. A causal relation was suggested by the finding that oxidative metabolism was normal in a group of HLP subjects whose lipid levels were lowered by treatment with cholestyramine.

Arteriosclerosis↗

PubMed1987

Intermediate-density lipoproteins and progression of coronary artery disease in hypercholesterolaemic men.

Lipoprotein mass concentrations were measured by analytical ultracentrifugation in a subset of 57 hypercholesterolaemic male participants in the National Heart, Lung, and Blood Institute Type II Coronary Intervention Study. 2-year changes in levels of intermediate-density lipoproteins (IDL) of flotation rate 12-20 were strongly predictive of progression of coronary artery disease at 5 years. Changes in serum mass concentrations of low-density lipoproteins (LDL; flotation rate 0-12), very-low-density lipoproteins (VLDL; flotation rate 20-400), high-density lipoproteins (HDL), and the HDL2 and HDL3 subfractions did not differ significantly between men with and without definite progression of coronary artery disease. The relation of IDL mass to disease progression remained significant (p less than 0.05) after adjustment for group assignment to cholestyramine treatment or placebo and was only slightly reduced (p less than or equal to 0.06) by adjustment for changes in LDL mass concentrations. Changes in IDL mass and ratios of HDL-cholesterol to total-cholesterol or LDL-cholesterol were inversely correlated and had a similar ability to predict progression. The findings are consistent with earlier evidence that IDL are directly involved in the development of coronary artery disease and suggest that ratios of HDL-cholesterol to total-cholesterol or LDL-cholesterol may be indicators of coronary disease risk partly owing to relations with IDL metabolism.

Adult↗

PubMed1994

Effect on coronary atherosclerosis of decrease in plasma cholesterol concentrations in normocholesterolaemic patients. Harvard Atherosclerosis Reversibility Project (HARP) Group.

Lipid-lowering therapy ameliorates coronary atherosclerosis in patients with raised concentrations of low-density-lipoprotein (LDL) cholesterol. We have investigated whether a similar benefit can be obtained in normocholesterolaemic patients. We studied 79 normocholesterolaemic patients with coronary heart disease (70 male, 9 female), mean age 58 years, all non-smokers, with mean total cholesterol concentration 5.5 mmol/L. All patients received diet therapy and were randomly assigned placebo (39) or active treatment (40) with pravastatin, nicotinic acid, cholestyramine, and gemfibrozil stepwise as needed to reach the specified goal (total cholesterol < or = 4.1 mmol/L, ratio of LDL/high-density-lipoprotein [HDL] cholesterol < or = 2.0). Coronary angiograms at baseline and after 2.5 years of treatment were analysed by computer-assisted quantitative techniques. There was no significant difference in coronary atherosclerosis during follow-up between the active treatment and placebo groups; the mean minimum diameter narrowed significantly but to the same extent in both groups (change baseline to 2.5 years 0.14 [SD 0.42] and 0.15 [0.42] mm, respectively, both p < 0.001). Similarly, the change in percentage stenosis did not differ between the groups (2.1 [10.6] vs 2.4 [10.3]%). By multiple regression analysis, the adjusted difference between the groups was a 0.04 mm (95% CI -0.04 to 0.12 mm) increase in minimum diameter and a 0% (-1.7 to 1.7) change in percentage stenosis. The groups differed significantly in plasma lipids (% change in active minus % change in placebo group: -28% total cholesterol, -41% LDL-cholesterol, 13% HDL-cholesterol, -26% triglycerides, -31% apolipoprotein B, all p < 0.001). Thus, intensive pharmacological treatment of normocholesterolaemic patients has significant effects on plasma lipid concentrations but no angiographically measurable benefit on the coronary arteries.

Anticholesteremic Agents↗

PubMed1985

Management of paucity of interlobular bile ducts.

Two types of paucity of interlobular bile ducts (PIBD) may be observed in children with chronic cholestasis. The syndromatic type (80 cases) is the most frequent. The non-syndromatic type (32 cases) is the most severe and half of the patients in this group died from liver failure in the first years of life. The main therapeutic point is that patients with PIBD should not be operated on. The only treatment available is symptomatic medical treatment: the main helpful possibilities concern feeding of medium-chain triglycerides, large supplementation of liposoluble vitamins (A, D, E and K) given intramuscularly, phenobarbital and cholestyramine when there is severe pruritus. The place of the liver transplantation will be clarified in the near future.

Bile Ducts, Intrahepatic↗

PubMed1987

The effect of prostaglandins, branched-chain amino acids and other drugs on the outcome of experimental acute porcine hepatic failure.

Prostaglandins, N-acetyl-cysteine, cholestyramine and essential phospholipids have all been shown to protect experimental animals from severe hepatic damage in various models when used prophylactically. Silibinin has been used in the treatment of Amanita phalloides poisoning. Branched-chain amino acids have been recommended in acute hepatic failure. We have used all these forms of therapy at the time of initiation of hepatic failure in a reliable pig model. Of the above, only prostaglandins have been shown to reverse the effects of the hepatic insult in terms of prolonged survival and histological changes. Although conventional liver function tests and plasma amino acids in prostaglandin-treated animals are not improved, cerebrospinal fluid amino acids remain normal, in contrast to the other groups of untreated and treated hepatic failure animals.

Acetylcysteine↗

PubMed1981

Pseudomembranous (antibiotic-associated) colitis.

We have come to understand the cause of antibiotic-associated pseudomembranous colitis (PMC) only in the last decade. Clostridium difficile produces the intestinal dysfunction and the characteristic finding of exudative plaques on the mucosa by elaborating a toxin in the colon. This report reviews the development of our knowledge of this disease and the rapid adoption of a rational therapy once the cause was specified. C. difficile or its toxin can be cultured or isolated from the stools of 90% of the patients with PMC. This organism is almost never found in healthy people or in any other conditions except inflammatory bowel disease, where its significance is not yet known. The detection of pseudomembranes by sigmoidoscopy establishes the diagnosis. The laboratory technics that confirm the presence of C. difficile and its toxin are being incorporated into many laboratories around the country. Treatment of diagnosed PMC is relatively simple and usually completely effective. The offending antibiotic is stopped, a proper fluid and electrolyte balance maintained, and oral vancomycin begun, 125 to 500 mg four times a day. Cholestyramine can also be used as an adjunct to this regimen. Relapse can occur in patients treated with oral vancomycin, necessitating a repeat course of therapy.

Anti-Bacterial Agents↗

PubMed1985

Pharmacokinetic interactions between digoxin and other drugs.

Drug interactions with digoxin are important because of this agent's narrow therapeutic index. Among the drugs that can decrease digoxin bioavailability are cholestyramine, antacid gels, kaolin-pectate, certain antimicrobial drugs and cancer chemotherapeutic agents. In selected patients, antibiotics may enhance digoxin bioavailability by eliminating intestinal flora that metabolize digoxin. Antiarrhythmic drugs, such as quinidine and amiodarone, can markedly increase steady state serum digoxin levels. Certain calcium channel blocking drugs, particularly verapamil, have a similar effect. Potassium-sparing diuretic drugs, such as spironolactone, can alter digoxin pharmacokinetics. Indomethacin may decrease renal excretion of digoxin in preterm infants. Finally, rifampin, an antibiotic used in the treatment of tuberculosis, may lower steady state serum digoxin levels in patients with severe renal disease. Physicians must maintain constant vigilance whenever medications are added to or withdrawn from a therapeutic regimen that includes digoxin.

Antacids↗

PubMed2002

Loss of nuclear receptor SHP impairs but does not eliminate negative feedback regulation of bile acid synthesis.

The in vivo role of the nuclear receptor SHP in feedback regulation of bile acid synthesis was examined. Loss of SHP in mice caused abnormal accumulation and increased synthesis of bile acids due to derepression of rate-limiting CYP7A1 and CYP8B1 hydroxylase enzymes in the biosynthetic pathway. Dietary bile acids induced liver damage and restored feedback regulation. A synthetic agonist of the nuclear receptor FXR was not hepatotoxic and had no regulatory effects. Reduction of the bile acid pool with cholestyramine enhanced CYP7A1 and CYP8B1 expression. We conclude that input from three negative regulatory pathways controls bile acid synthesis. One is mediated by SHP, and two are SHP independent and invoked by liver damage and changes in bile acid pool size.

Animals↗

PubMed1982

Cholesterol biosynthesis and modulation of membrane cholesterol and lipid dynamics in rat intestinal microvillus membranes.

Experiments were performed to test the hypothesis that cholesterol biosynthesis in the rat ileal enterocyte, the major absorptive cell lining the distal epithelium of the small intestine, can modulate the cholesterol content and the motional freedom of the plasma membrane lipids. Decreased sterol biosynthesis in vivo was elicited by feeding sodium taurocholate or by fasting the rats, whereas increased synthesis was induced by biliary ligation or feeding cholestyramine, a bile salt binding resin; these effects were monitored by assay of mucosal 3-hydroxy-3-methylglutaryl coenzyme A reductase. After each procedure, isolated microvillus membranes were examined to determine the lipid composition and the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene. The results demonstrate that variations in cholesterol biosynthesis in vivo can modulate the cholesterol content and the motional freedom of the lipids of the microvillus membrane; similar effects were not observed on the basolateral membrane. The observations suggest that the normal pattern of decreased lipid motional freedom in microvillus membranes of the distal as compared to the proximal small intestine of the rat results from higher rates of cholesterol biosynthesis in the distal mucosa.

Animals↗