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PubMed1972

Effect of cholestyramine on bile acid metabolism in normal man.

The effect of cholestyramine administration on the enterohepatic circulation of bile acids was studied in eight normal volunteers. In six subjects the metabolism of sodium taurocholate-(14)C was determined after its intravenous injection before and during the 6th wk of cholestyramine administration, 16 g/day. In two subjects, the metabolism of cholic acid-(14)C was observed before and during the 2nd wk of cholestyramine, 16 g/day. Bile acid sequestration resulted in a more rapid disappearance of the injected primary bile acid and its metabolic products. The composition of fasting bile acids was promptly altered by cholestyramine to predominantly glycine-conjugated trihydroxy bile acid. In four subjects, unconjugated bile acid-(14)C was administered during cholestyramine administration; the relative proportion of glycine-conjugated bile acid-(14)C before enterohepatic circulation was similar to the relative proportion of unlabeled glycine-conjugated bile acid present in duodenal contents after an overnight fast, indicating that a hepatic mechanism was responsible for the elevated ratios of glycine- to taurine-conjugated bile acid (G: T ratios) observed. The relative proportions of both dihydroxy bile acids, chenodeoxycholic and deoxycholic, were significantly reduced. Steatorrhea did not occur, and the total bile acid pool size determined after an overnight fast was unaltered by cholestyramine. These findings suggest that in normal man bile acid sequestered from the enterohepatic circulation by cholestyramine is replaced by an increase in hepatic synthesis primarily via the pathway leading to production of glycocholic acid.

Adult↗

PubMed1979

Effects of neomycin alone and in combination with cholestyramine on serum cholesterol and fecal steroids in hypercholesterolemic subjects.

Effects of neomycin were studied on serum cholesterol and fecal steroids in hypercholesterolemic patients during a short treatment period (4 wk) and a long treatment period (16 mo), using small (1.5 g/d) and large (up to 6 g/d) doses alone and in combination with cholestyramine. In the short-term low-dose study the decrease in serum cholesterol by 21% was associated with a proportionate increase in fecal cholesterol elimination as neutral sterols through impaired cholesterol absorption. Serum cholesterol remained low and fecal steroid excretion remained elevated in the long-term neomycin study. Increasing the dosage from 1.5 to 6 g/d at the end of the 16-mo period brought about a further slight decrease in serum cholesterol and a small further increase in fecal neutral and acidic steroids. The increases in fecal bile acids and fat but not in neutral sterols were positively correlated with the increases in the neomycin dosage. Thus, large neomycin doses can also cause bile acid malabsorption. In another series of patients, a decrease (25%) in serum cholesterol by cholestyramine was associated with a proportional increase in the fecal elimination of cholesterol (2.5-fold) as bile acids. The inclusion of neomycin in cholestyramine therapy further increased fecal steroid output (solely as neutral sterols) by only about one-fifth of that due to cholestyramine, but further decreased serum cholesterol almost to the same extent (-17%) as cholestyramine alone. The overall decrease was 38%, no side effects occurred, and the patients found combination therapy convenient. Neomycin decreased serum cholesterol in different studies by 10+/-2, 17+/-4, and 12+/-4% per 100 mg/d of the increment in fecal steroids, the respective decrease for cholestyramine being only 2.2+/-0.5%. Thus, neomycin effectively reduced serum cholesterol by a relatively small increase in cholesterol elimination (via cholesterol malabsorption) compared with cholestyramine-induced bile acid malabsorption.

Adult↗

PubMed1975

The single dose method of administering cholestyramine.

A new and simplified method for the administration of cholestyramine is presented. It has been our finding that the total daily dose of the resin (as indicated below) may be administered once a day in a single dose at any time during the waking hours, without reference to meals, and the resulting degree of cholesterol lowering is as great or greater than that obtained by the same dose with the traditional method of t.i.d. administration of cholestyramine. Doses of 12 or 16 gm per day, have been administered as a single dose to adult patients. We have not encountered side effects from the administration of this resin as a single dose, however an occasional patient has objected to the volume involved, and has preferred to take a smaller volume 2 or 3 times daily. Because of the bulk involved in the administration of larger doses, we have found it expedient to give doses of 24 gms per day by dividing the dose in half and administering it twice daily without reference to meals. The 21 patients in our study who received cholestyramine in the single daily dose obtained an average reduction of their serum cholesterol of 21.58% over baseline values. Twenty patients receiving a somewhat larger dose, administered twice daily (b.i.d. dose), obtained a 27.57% reduction in the serum cholesterol, and out of this entire series there were 22 patients who had at other times received the cholestyramine by the t.i.d. regimen. They had obtained a 25.61% reduction of their serum cholesterol (by the t.i.d. regimen). All 3 average percent reductions compared to 0 are highly significant (p is less than 0.0001). One hundred forty out-patients treated by the conventional t.i.d. program of administration obtained a 16.8% reduction in the serum cholesterol. This includes some patients taking relatively small and less effective doses. Our entire series of 238 patients (to be reported subsequently) treated as out-patients have obtained an average reduction of 22% of their serum cholesterols. There has been no statistically significant influence on the levels of the serum triglycerides during cholestyramine therapy in this series (results on 69 patients showed an average rise of 5.9 mg per 100 ml in the serum triglycerides). See discussion in text. Some studies have indicated a rise of serum triglycerides during cholestyramine therapy. It is recommended that triglycerides be monitored periodically during the course of cholestyramine treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Cholesterol↗

PubMed1988

Clinical experience with simvastatin compared with cholestyramine.

Simvastatin (MK733), derived from lovastatin by substituting CH3 for H at the 2' position, is a potent hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitor. Its cholesterol-lowering effect in 40 patients with heterozygous familial hypercholesterolaemia was more pronounced (an LDL-cholesterol reduction of 43%) than that of cholestyramine monotherapy in a matched group of 20 patients (30% reduction). The combination of the 2 drugs for 50 patients who tolerated cholestyramine was even more effective (a 54% reduction of LDL-cholesterol). The other changes were as follows: total cholesterol (simvastatin [S] -36%, cholestyramine [C] -23%, both drugs in combination [S + C] -45%); HDL-cholesterol (S +16%, C +9%, S + C +20%); triglyceride (S -21%, C +11%, S + C -17%); and the apolipoprotein B/apolipoprotein A ratio (S -51%, C -39%, S + C -67%). Cholestyramine caused more gastrointestinal adverse effects (12 of 20 patients), whereas a transaminase increase was seen both with cholestyramine (2 of 20 patients) and simvastatin (3 of 40 patients) and with the combination (6 of 50 patients). Treatment with simvastatin decreases the atherogenic potential of plasma more than cholestyramine monotherapy and causes fewer adverse effects. For those patients who tolerate cholestyramine, the combination of the drugs is even more potent.

Adult↗

PubMed1988

A comparison of the lipid-lowering and intestinal morphological effects of cholestyramine, chitosan, and oat gum in rats.

Cholestyramine, chitosan, and oat gum are lipid-lowering compounds. Cholestyramine use in humans may contribute to colonic adenocarcinoma; chitosan and oat gum are being studied in the rat to determine their potential for human use. To compare these compounds, we fed three groups of 10 male Sprague-Dawley rats one of the substances at 5% of diet with 1% cholesterol and 0.2% cholic acid; two other groups were fed cellulose with and without 1% cholesterol and 0.2% cholic acid. All groups had similar food intake and weight gains. Cholesterol feeding increased total liver lipids almost 3-fold and liver cholesterol concentration almost 10-fold. Cholestyramine, oat gum, and chitosan all significantly lowered liver cholesterol with cholestyramine feeding yielding levels identical to the noncholesterol-fed basal group. Chitosan and oat gum lowered liver cholesterol moderately. Cholestyramine and chitosan both significantly lowered serum cholesterol compared to the cellulose group. Oat gum was less effective. Hemoglobin and serum iron were similar in all groups except the oat gum group, which had decreased serum iron. Histological examination of small and large bowel with morphometry revealed statistically significant increases in both proximal and distal small bowel and distal large bowel mucosal thickness in the cholestyramine-fed group. No changes were noted in the proximal large bowel. Neither chitosan nor oat gum produced mucosal change other than an increase in the distal small bowel with the oat gum diet. Chitosan may have lipid-lowering effects similar to those of cholestyramine without the deleterious changes in intestinal mucosa.

Animals↗

PubMed1991

[Stimulation of the fecal excretion of polychlorinated biphenyls (KC-600) by diets containing rice bran fiber and cholestyramine].

Among the eight kinds of dietary fiber tested, rice bran fiber (RBF) mostly bound Kanechlor 600 (PCB) in vitro. The PCB bound to dietary fiber was in proportion to the lignin content in dietary fiber. We investigated whether RBF, lignin, cholestyramine and their combination stimulate the fecal excretion of PCB in rats. In the group fed a diet containing 10% (w/w) RBF, fecal excretion of PCB was stimulated. In the group fed a diet containing 10% (w/w) RBF and 5% (w/w) cholestyramine, more PCB was excreted in the feces. However, the group fed a diet containing 10% (w/w) RBF and 5% (w/w) lignin excreted the same amount of PCB as the group fed a diet containing 10% (w/w) RBF. The total PCB excreted into the feces for 21 days in the groups fed 10% (w/w) RBF, 10% (w/w) RBF and 5% (w/w) lignin, 5% (w/w) cholestyramine and 10% (w/w) RBF and 5% (w/w) cholestyramine diet was 3.4, 3.8, 2.3 and 5.7 times, respectively, that of the control. The stool transit time of rats fed 10% (w/w) RBF and 5% (w/w) cholestyramine diet was one hour faster than that of rats fed a 5% (w/w) cholestyramine diet. Therefore, we concluded that RBF has the greatest effect when administered in combination with cholestyramine on the fecal excretion of PCB.

Animals↗

PubMed1989

Comparison between low-dose simvastatin and cholestyramine in moderately severe hypercholesterolemia.

In a 6-week multicenter study, we compared the efficacy and tolerance of a treatment with 10 mg of simvastatin, a new inhibitor of the HMG-CoA reductase to that of 12 g cholestyramine in 145 patients whose total cholesterol remained between 250 and 350 mg/dl after 4 weeks of a standard lipid-lowering diet. The decrease in total cholesterol reached 21% in the simvastatin group and 16% in the cholestyramine group (p less than 0.01) while the LDL-cholesterol decreased respectively by 30% and 25%. HDL cholesterol increased by 11% in the simvastatin group and by 7% in the cholestyramine group. The ratios of total to HDL cholesterol and LDL to HDL cholesterol decreased by 28.1% and 35.8% respectively with simvastatin and by only 19.5% and 27.9% respectively with cholestyramine. Triglycerides decreased by 5.8% with simvastatin and increased by 8.5% with cholestyramine. Significantly less adverse experiences were observed with simvastatin than with cholestyramine. Simvastatin at the dosage of 10 mg appeared to be at least as efficient as 12 g of cholestyramine and generally better tolerated.

Adolescent↗

PubMed1982

Fenofibrate and cholestyramine in type II hyperlipoproteinaemia.

The effect of fenofibrate (300-600 mg daily) was compared with cholestyramine (12 g daily) in 13 patients with primary type II hyperlipoproteinaemia. Seven of the patients had monogenic familial hypercholesterolaemia. Both fenofibrate (21.0%) and cholestyramine (18.5%) decreased serum cholesterol level. Fenofibrate (22.7%) and cholestyramine (19.6%) had equally decreasing effects on LDL-cholesterol, but fenofibrate increased HDL-cholesterol (10.4%), although not significantly, whereas cholestyramine decreased the HDL-cholesterol (11.9%). Therefore the ratio of HDL-cholesterol to total cholesterol was higher after fenofibrate (0.17) than after cholestyramine (0.13). Serum triglyceride concentration decreased by 57.1 per cent during six months' treatment with fenofibrate, but returned to a higher level during 3 months' cholestyramine treatment. When the dose of fenofibrate was increased from 300 mg to 600 mg daily, serum cholesterol, LDL-cholesterol, and triglyceride values decreased, and HDL-cholesterol and the ratio of HDL-cholesterol to total cholesterol increased, but only in patients with non-familial hypercholesterolaemia. Fenofibrate is in addition to cholestyramine an useful hypolipidaemic drug in type II hyperlipoproteinaemia.

Adult↗

PubMed1980

Cholesterol absorption in man: effect of administration of clofibrate and/or cholestyramine.

Cholesterol absorption measurements were carried out in a free-living out-patient population by a plasma isotope-ratio method previously validated for in-patients (Samuel, P., J. R. Crouse and E. H. Ahrens, Jr., 1978. J. Lipid Res. 19: 82-93). To test the reproducibility of the method in out-patients, 18 patients were tested twice: the mean intra-assay variability was +/- 6.0%. The method was then applied in 150 hyperlipidemic male out-patients, ingesting a standardized diet containing 250mg cholesterol per day, who had been randomized into four different drug-treatment groups: 1) no medication, 2) clofibrate, (2g/day), 3) cholestyramine (16g/day), or 4) both clofibrate and cholestyramine. Cholesterol absorption (as percent of the oral dose) was increased in patients receiving cholestyramine (P < 0.02) and decreased in those receiving clofibrate (P < 0.02); the group on the combined medication had the same pecent absorption as the control group. In twelve patients receiving cholestyramine, a second test of cholesterol absorption was performed 30 min after each patient had received 8g of cholestyramine. The pre-test administration of cholestyramine caused a 38% decrease in cholesterol absorption (P < 0.001), compared to results obtained when medication was withheld prior to testing. These results demonstrate that the isotope-ratio method of measuring cholesterol absorption is a reproducible procedure applicable to a free-living out-patient population, and that the hypolipidemic drugs, clofibrate and cholestyramine, significantly affect cholesterol absorption in man. The data also show that the results of measurements of cholesterol absorption can be profoundly altered by the type and timing of medication in relationship to the test meal of labeled cholesterol.

Absorption↗

PubMed2001

Reduced susceptibility of low density lipoprotein to lipid peroxidation after cholestyramine treatment in heterozygous familial hypercholesterolemic children.

Cholestyramine treatment in children with heterozygous familial hypercholesterolemia (FHHe) can interfere with fat absorption from the intestinal tract, and has the potential to decrease the absorption of fat-soluble vitamins. The aim of this study was to examine the effect of cholestyramine treatment on the levels of the fat soluble vitamins (vitamin E, beta-carotene and lycopene) in LDL, on the glutathione system and on the susceptibility of LDL to oxidation in FHHe children. Patients were 16 children (seven girls, nine boys), age 14+/-4 years, non-smokers. Plasma LDL level before cholestyramine treatment but after dietary treatment was 239+/-50 mg% with no secondary cause for hypercholesterolemia. A control group was comprised of ten children (seven girls, three boys), age 14+/-4 years with plasma LDL level of 100+/-14 mg%. Blood was drawn from 16 FHHe children and five control children after fasting for 14 h. Thereafter cholestyramine treatment was begun in the patient group, at a dose of 8 g/day for 2 months. At the end of this period the dose was increased to 12-16 g/day for an additional 2 months. After 4 months from the beginning of the treatment, blood was drawn again. Plasma LDL cholesterol decreased after treatment by 14% (from 239+/-67 mg% before treatment to 205+/-55 mg% after treatment, P=0.07). Malondialdehyde (MDA) levels measured by thiobarbituric reactive substances (TBARS) assay in LDL at the end of oxidation were 30% higher in FHHe children in comparison to controls (P=0.02). After treatment TBARS levels in LDL (after in vitro oxidation) from FHHe children were decreased by 23% (P=0.02). Vitamin E levels in LDL from FHHe children after treatment were decreased by 65%, while beta-carotene and lycopene contents in LDL, paradoxically increased by 90 and 102%, respectively. In red blood cells (RBC), glutathione peroxidase (GPx) and glutathione transferase (GTf) activities were decreased by 29 and 24%, respectively, while glutathione reductase activity, total and oxidized glutathione contents from FHHe children did not change after cholestyramine treatment. LDL was more prone to oxidation in FHHe children than in controls, when measured by TBARS levels after LDL oxidation (with 10 &mgr;M CuSO(4)). Cholestyramine treatment for 4 months normalized LDL susceptibility to oxidation measured by TBARS levels, despite the decrease in vitamin E content in LDL from treated FHHe children. This is presumably due to the increased LDL content of beta-carotene and lycopene after treatment. GPx and GTf activities decreased after treatment, presumably due to the drop in oxidative stress within the RBCs, in parallel to the decreased LDL tendency to oxidation. Cholestyramine treatment in FHHe children has an overall antioxidant effect on LDL.

Journal Article↗

PubMed1977

Interruption of the enterohepatic circulation of phenprocoumon by cholestyramine.

The effect of cholestyramine (12 gm/day divided into 3 doses) on the pharmacokinetics and pharmacodynamics of a single intravenouse dose (30 mg) of phenprocoumon was studied in 6 normal subjects. Cholestyramine treatment led to an increase in the rate of elimination of phenprocoumon in all. Total clearance increased 1.5- to 2-fold. The total anticoagulant effect per dose was considerably reduced during treatment with cholestyramine. Binding studies in vitro showed that phenprocoumon is strongly bound to cholestyramine and that at a given cholestyramine concentration the percentage of phenprocoumon bound remained constant over a large concentration range of phenprocoumon. The results suggest that phenprocoumon undergoes extensive enterohepatic recycling in man which can be effectively interrupted by cholestyramine.

4-Hydroxycoumarins↗

PubMedDate not supplied

A steady-state evaluation of the effects of propantheline bromide and cholestyramine on the bioavailability of digoxin when administered as tablets or capsules.

Drug interactions can profoundly alter the absorption of digoxin in tablet form. This study evaluated whether digoxin solution in capsules, a new dosage form with 90% to 100% bioavailability, would reduce such alterations, specifically those caused by cholestyramine and propantheline bromide. The investigation used a six-treatment, steady-state, balanced, incomplete block design with 18 healthy adults studied for four continuous two-week treatment periods. Treatments were either two 0.25 mg digoxin tablets or two 0.20 mg digoxin capsules administered alone, with propantheline, 15 mg qid, or with cholestyramine, 8 g qd. Bioavailability was determined from steady-state, 24-hour area under the serum concentration-time curve (AUC, ng X h/mL) and from 0- and 24-hour trough serum digoxin concentrations (ng/mL). The AUCs for tablets alone, with cholestyramine, and with propantheline were 32.8 +/- 13.3 (+/- SD), 22.4 +/- 12.1, and 40.6 +/- 13.9, respectively, while corresponding values for capsules were 31.7 +/- 9.3, 24.7 +/- 7.9, and 35.9 +/- 12.8. The trough concentrations for tablets alone, with cholestyramine, and with propantheline were 0.88 +/- 0.47, 0.61 +/- 0.38, and 1.09 +/- 0.35, respectively; trough concentrations for capsules were 0.77 +/- 0.28, 0.74 +/- 0.28, and 0.96 +/- 0.48, respectively. The only significant differences in AUC were seen when comparing tablets alone versus tablets with cholestyramine (P less than .0005) and tablets with propantheline (P less than .01). A significant finding was also observed when comparing trough concentrations for tablets alone versus tablets with cholestyramine (P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Cholestyramine alters the lipid and energy metabolism of chicks fed dietary medium- or long-chain triacylglycerol.

The effects of cholestyramine, a bile acid binding polymer, on the lipid and energy metabolism of chicks given dietary medium-chain triacylglycerol (MCT) or long-chain triacylglycerol (LCT) were investigated. Chicks (from 8 to 17 days of age) were fed diets containing MCT or LCT at 200 g oil/kg diet with or without 2% cholestyramine under equalized feeding conditions. An adjusted LCT diet was formulated in order to supply another group with daily nutrients and dietary metabolizable energy (ME) equal to MCT groups, except for corn starch. ME intakes of chicks given MCT or LCT diets were reduced by cholestyramine; consequently, fat and energy retention was reduced, though the reduction was more drastic in chicks fed LCT. This was caused by a change in amounts of the fecal excretion of fat and bile acids. Cholestyramine enhanced the excretion of octanoic acid (8:0) in the feces, which suggests that bile acids are needed for 8:0 absorption. Cholestyramine affects the utilization of dietary MCT and LCT by lowering fat and energy retention in chicks. However, the effect of cholestyramine on MCT utilization was smaller than its effect on utilization of LCT.

Animals↗

PubMed1995

Resistant starch is more effective than cholestyramine as a lipid-lowering agent in the rat.

Amylase-resistant starch (RS) represents a substrate for the bacterial flora of the colon, and the question arises as whether RS shares with soluble fibers common mechanisms for their lipid-lowering effects. It is uncertain whether a cholesterol-lowering effect depends basically on an enhanced rate of steroid excretion or whether colonic fermentations also play a role in this effect. In the present study, the effect of RS (25% raw potato starch), of a steroid sequestrant (0.8% cholestyramine), or both were compared on bile acid excretion and lipid metabolism in rats fed semipurified diets. RS diets led to a marked rise in cecal size and the cecal pool of short-chain fatty acids (SCFA), as well as SCFA absorption; cholestyramine did not noticeably affect cecal fermentation. Whereas cholestyramine was particularly effective at enhancing bile acid excretion, RS was more effective in lowering plasma cholesterol (-32%) and triglycerides (-29%). The activity of 3-hydroxy-3-methylglutaryl-CoA reductase was increased fivefold by cholestyramine and twofold by RS. This induction in rats fed RS diets was concomittant to a depressed fatty acid synthase activity. In rats fed the RS diet, there was a lower concentration of cholesterol in all lipoprotein fractions, especially the (d = 1.040-1.080) fraction high-density lipoprotein (HDL1), while those fed cholestyramine had only a significant reduction of HDL1 cholesterol. In contrast to cholestyramine, RS also depressed the concentration of triglycerides in the triglyceride-rich lipoprotein fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Amylases↗

PubMed1985

Effects of combination cholestyramine-neomycin treatment on plasma lipoprotein concentrations in type II hyperlipoproteinemia.

Recent prospective clinical trials have established that cholesterol reduction in patients with elevated (upper 90th percentile) concentrations of low-density lipoproteins (LDL) reduces the incidence of myocardial infarction and sudden death. Because the level of protection from these cardiovascular sequelae is directly related to the degree of LDL reduction, combination therapy using different hypolipidemic agents has been used in patients with type II hyperlipoproteinemia (HLP). Neomycin is as effective as cholestyramine in reducing LDL levels and combination neomycin-niacin treatment normalizes the plasma lipoproteins in 92% of patients with type II HLP. Because neomycin could theoretically ameliorate some of the gastrointestinal side effects of cholestyramine in addition to further affecting cholesterol levels, the effects of combination cholestyramine-neomycin treatment on the plasma lipoprotein were assessed in 18 patients with type II HLP in a 9-month clinical trial. Compared with diet-only treatment, cholestyramine reduced total and LDL cholesterol levels by 77 mg/dl (22%) and 78 mg/dl (31%), respectively. In addition to relieving cholestyramine-induced constipation, neomycin further reduced the total cholesterol level by 20 mg/dl (6%). However, this further reduction in total cholesterol concentration was the result of a decrease in the concentration of high-density lipoprotein cholesterol. These findings indicate that combination therapy does not have an additive LDL cholesterol-lowering effect and that neomycin and cholestyramine is not a useful drug combination. In addition, these results illustrate the importance of determining the high-density lipoprotein cholesterol concentration to fully interpret the effects of hypolipidemic treatment.

Cholesterol, HDL↗

PubMed1987

Cholestyramine treatment in early life of low-density lipoprotein receptor deficient Watanabe rabbits: decreased aortic cholesteryl ester accumulation and atherosclerosis in adult life.

Effect of cholestyramine treatment in early life of Watanabe heritable hyperlipidemic rabbits (an animal model lacking low-density lipoprotein receptor activity) on subsequent (6 months recovery) occurrence of natural atherosclerotic lesion and arterial cholesterol metabolism was investigated. Initial cholestyramine treatment decreased both plasma total cholesterol and HDL-cholesterol levels which normalized within 4 weeks after treatment was discontinued. At 9 months of age (age of occurrence of spontaneous atherosclerotic lesions), the extent of aortic atherosclerosis in cholestyramine pre-treated animals was modestly lower (P less than 0.05), as compared to controls, with a significant (P less than 0.05) decrease in aortic cholesteryl ester content. Furthermore, at the end of the recovery period aortic activity of acyl-CoA: cholesterol acyltransferase and neutral cholesterol esterase activity was significantly (P less than 0.05) lower in cholestyramine-pretreated animals. These studies show that early cholestyramine pre-treatment in a low-density lipoprotein receptor-deficient animal model causes persistent changes which might influence cholesteryl ester accumulation and atherogenesis in adult life, even after cholestyramine treatment is discontinued.

Age Factors↗

PubMed1994

Effect of the interruption of enterohepatic circulation of bile acids by cholestyramine on apolipoprotein gene expression in the rat.

The aim of the study was to assess how the interruption of enterohepatic circulation may affect the regulation of apolipoprotein synthesis. For this purpose, apolipoprotein mRNA levels were measured in the liver and small intestine of male Wistar rats fed for 3 weeks diets with or without cholestyramine (5% w/w). In order to modulate intestinal lipid flux, we used diets with 2 or 10% lipid content. Cholestyramine treatment decreased plasma triglyceride and cholesterol concentrations (by 63% and 32%, respectively) in rats fed 10% corn oil containing diet but had no significant effect on plasma lipids in rats fed a low-fat diet. Plasma apo B and apo A-IV concentrations were lowered by cholestyramine treatment in both 10 and 2% oil fed groups; however plasma apo E concentration was only affected in rats receiving 10% corn oil in the diet. Cholestyramine treatment had no significant effect on plasma apo A-I concentration. Hepatic apo B, apo E and apo A-IV mRNA levels were similar among dietary groups. Cholestyramine administration caused an increase in hepatic apo A-I mRNA level only in rats fed low-fat diet. In the intestine cholestyramine treatment decreased apolipoprotein mRNA levels in jejunum but had a few effect on apolipoprotein mRNA levels in ileum. These experiments have shown that long-term decrease in the intraluminal availability of bile acids may alter not only lipid and lipoprotein metabolism but also the regulation of apolipoprotein synthesis.

Animals↗

PubMed1989

Effect of combined therapy with bezafibrate and cholestyramine on low-density lipoprotein metabolism in type IIa hypercholesterolemia.

This study was designed to examine the influence of combined therapy with bezafibrate and cholestyramine on plasma lipids and on the metabolism of low-density lipoprotein (LDL). Twenty-one type II hyperlipidemic subjects were treated with bezafibrate alone or in combination with cholestyramine. A 17% fall in plasma cholesterol was seen with bezafibrate, and addition of cholestyramine produced an additional 9% reduction in this lipid. The effectiveness of the combination therapy was mediated through a 47% decrement in very-low-density lipoprotein (VLDL) cholesterol, a 37% reduction in LDL cholesterol, and a 15% increase in the level of that lipid in high-density lipoprotein (HDL). Plasma triglyceride fell 43% when bezafibrate was given alone, and did not change further when cholestyramine was added. The metabolism of LDL was examined in nine individuals to determine the mechanism underlying these changes. No significant modification in LDL synthetic rate was incurred with either drug regimen, whereas the fractional catabolic rate of LDL via the receptor pathway rose by 66% with bezafibrate alone and by 79% (compared to baseline) following the addition of cholestyramine. Plasma HDL rose during bezafibrate therapy due to an increase in the HDL3 subfraction. Compositional analysis of LDL showed a reduction in cholesterol ester and an increase in triglyceride and phospholipid during combined drug therapy. These results demonstrate that combined therapy with bezafibrate and cholestyramine markedly improves the lipoprotein profile in type II hyperlipidemia. The drugs appear to be complementary in their actions upon the LDL receptor pathway.

Adult↗