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PubMed1988

Bile salt binding properties of commonly used gastrointestinal drugs: maalox, carafate, and questran.

We have validated a method to measure bile salt binding by Maalox (aluminum hydroxide and magnesium hydroxide), Carafate (sucralfate), and Questran (cholestyramine) in vitro. The method used in this study involves a correction for adherent water volume and thus provides a correct measure of bile salt binding. With this approach, we described the binding properties of Maalox, Carafate, and Questran. The bile salt binding capacities of Carafate and Maalox are limited and do not have physiological or pharmacological significance. On the other hand, we found that Questran has substantial bile salt binding capacity. At the recommended dosage, Questran could deplete the total bile salt pool. We also found that Carafate, although not used as an antacid, has buffering capacity (maintaining a pH of solution in the range 4.2-4.8) which might contribute to its effectiveness as an ulcer treatment drug.

Aluminum Hydroxide↗

PubMed1991

Increasing the in vitro bile acid binding capacity of diethylaminoethylcellulose by quaternization.

Diethylaminoethylcellulose (DEAE-cellulose) was quaternized with methyl iodide (DEAE-cellulose-CH3I), and its in vitro binding capacity for sodium glycocholate, at room temperature, in water, Tris-HCl buffer (0.0015-0.0050 M, pH 7.0), and aqueous NaCl (0.0025 M) was determined by reversed-phase HPLC. Quaternization increased the in vitro bile salt binding capacity of DEAE-cellulose. On a molar basis, the binding capacity was greater than that of cholestyramine, a cholesterol-lowering agent. Increasing the ionic strength of the medium decreased the binding capacities, as expected if ionic interactions are important. However, conversion of DEAE-cellulose-CH3I to its chloride form did not change the binding capacity. The bile salt binding capacity of DEAE-cellulose-CH3I was similar for both sodium cholate and sodium glycocholate.

Adsorption↗

PubMed2003

Weighting in instrumental variables and G-estimation.

We propose here a simple scheme to use information on compliance and prerandomization covariates to improve analysis of randomized trials with non-compliance. We use the data to determine the effect of randomization on treatment received among various strata defined by pretreatment covariates. When the effect of treatment received on the outcome of interest is the same across strata and pretreatment covariates predict non-compliance, weighting the estimating functions by the effect of randomization on treatment received can improve the precision of explanatory estimates of treatment effect and can increase the power of intent-to-treat tests of the null hypothesis. Efficiency gains under the weighting scheme are a simple increasing function of the variability of these weights. Such weighting schemes will often lead to improvements even when these conditions are not met. We use a randomized trial of cholestyramine to illustrate these points.

Cholesterol↗

PubMed1992

Statistical validation of intermediate endpoints for chronic diseases.

We discuss the implementation of a criterion due to Prentice for the statistical validation of intermediate endpoints for chronic disease. The criterion involves examining in a cohort or intervention study whether an exposure or intervention effect, adjusted for the intermediate endpoint, is reduced to zero. For example, to examine whether serum cholesterol level is an intermediate endpoint for coronary heart disease (CHD), we may investigate the effect of the cholesterol lowering drug cholestyramine on CHD incidence adjusted for serum cholesterol levels. We show that use of this criterion will usually demand some form of model selection. When the unadjusted exposure or treatment effect is less than four times its standard error, the analysis can usually lead only to a weak form of validation, a conclusion that the data are not inconsistent with the validation criterion. More significant unadjusted exposure effects offer the potential for stronger types of validation statement such as 'the intermediate endpoint explains at least 50 per cent (or 75 per cent) of the exposure effect'.

Biomarkers↗

PubMed1998

Determination of 7alpha-hydroxycholesterol in dog plasma by high-performance liquid chromatography with fluorescence detection.

A new method was developed for the determination of 7alpha-hydroxycholesterol (7-HC) in dog plasma by means of high-performance liquid chromatography (HPLC) with fluorescence detection. 7-HC extracted with organic solvent from plasma was purified with Bond Elut 2OH and converted to a sensitive fluorescent derivative containing double coumarin groups at the C-3 and C-7 positions of the steroid nucleus with 7-methoxycoumarin-3-carbonyl azide. After removal of the excess reagent with Bond Elut NH2, the 7-HC derivative was separated by reverse-phase HPLC method. The detection limit of the authentic 7-HC-3,7-coumarin derivative was 4 pg (S/N = 5), approximately four times less than that of the 7-HC-3-anthroyl derivative yielded by reaction of 7-HC with 1-anthroylcyanide. The newly developed method was used to investigate the effects of consecutive oral administrations of cholestyramine (CA) on 7-HC levels in dog plasma. The plasma 7-HC levels of the CA-treated group were two times greater than those of the control group.

Animals↗

PubMed1996

Coordinate regulation of bile acid biosynthetic and recovery pathways.

Intestinal and hepatic recovery of bile acids is principally mediated by sodium dependent bile acid transporters. Of these, the ileal sodium bile acid transporter (isbt) and the hepatic sodium bile acid cotransporting polypeptide (ntcp) may be most important in determining the efficiency of bile acid recovery within the enterohepatic circulation. We used molecular probes to explore the relationship between the bile acid recovery pathway, at the level of isbt and ntcp, and the biosynthetic pathway, at the level of cholesterol 7 alpha-hydroxylase (cyp7). Taurocholate feeding of mice suppressed ntcp, isbt, and cyp7 mRNA levels as compared to controls. Cholestyramine feeding induced both cyp7 and isbt mRNA gene expression. Cholesterol feeding induced cyp7 mRNA levels but suppressed isbt gene expression. These results suggest that in mice the bile acid recovery and biosynthetic pathways are coordinately regulated, and these pathways may be responsive to the size of the bile acid pool in the enterohepatic circulation.

Animals↗

PubMed1985

The role of bile acids in the effect of ethinylestradiol on the biliary excretion of exogenous organic anions.

Ethinylestradiol (EE) has a cholestatic effect and decreases the biliary excretion of xenobiotics. In the present experiments, pretreatment with EE did not influence the biliary excretion of bile acids. On the other hand, the effect of EE on the biliary excretion of exogenous organic anions and on bile production was not influenced by administration of taurocholic acid (TC) or by depletion of bile acids by cholestyramine (CHOL). However, phenobarbital (PB) administered simultaneously with EE prevented the depressive effects of EE on the biliary flow and biliary excretion rate of rose bengal (RB). These results indicate that bile acids do not play an important role in the effects of EE and that changes in the bile salt independent fraction might be responsible for the effects of EE pretreatment on the biliary excretion of exogenous organic anions.

Animals↗

PubMed1981

Preventive effect of some substances on experimental oxalic calculogenesis in the frog.

Rana esculenta tadpoles that are fed spinach develop an oxalic calculogenesis. The addition of cholestyramine, orthophosphate, citrate, allopurinol and tungstate to the tank water prevented calculi formation while succinimide, magnesium oxide, hydrochlorothiazide and tetracycline were ineffective. Methylene blue proved lethal to tadpoles, and its anti-lithogenic activity could not be assessed. These findings, except for the non-effectiveness of magnesium oxide, are in agreement with both the theoretical expectations and the results obtained in other experimental models. Experimental frog calculogenesis seems to be a simple and valid method for evaluating anti-lithogenic activity.

Allopurinol↗

PubMed1976

The circadian rhythm of synthesis and catabolism of cholesterol.

The circadian rhythms of HMG-CoA reductase and cholesterol-7 alpha-hydroxylase (low values, during light, rising in the evening with maximum at 12.00 p.m.) are investigated in rats under diverse conditions. Intragastral administration of cholestyramine (bile acid-absorbing resin) leads to an increased rhythm of both enzymes. Feeding of cholic acid (or cholesterol) reduces the activity of both enzymes (of HMG-CoA reductase and cholesterol-7 alpha-hydroxylase, respectively). In starved rats enzyme activity and time of day is proportional to the metabolism of a substrate.ies are lowered, too; a damped rhythm reappears after 24 h. A 20% fat diet (containing saturated fatty acids predominantly) markedly reduces the high values. Enzyme activities inhabited after thyroidectomy can be normalized by thyroxin substitution. Thyroxin administration in the normal remains without effect. Four-day insulin treatment of the normal inhibits cholesterol-7 alpha-hydroxylase, has no effect on HMG-CoA reductase. In the untreated diabetic rat cholesterol-7 alpha-hydroxylase is increased, HMG-CoA reductase significantly inhibited. Insulin treatment of the diabetic animal results in normalized values of HMG-CoA reductase whilst cholesterol-7 alpha-hydroxylase is nearly completely suppressed. The rate-limiting enzymes of cholesterol turnover are peripherally regulated by their products via a negative feedback. In contrast, hormones may have synergistic or opposite effects; thus they may represent means of higher regulation. All regulative possibilities discussed (except hypophysectomy) do modifiy the circadian rhythms. This cannot be demonstrated after hypophysectomy. After hypophysectomy circadian rhythms are not detectable any more. To get valid data about biochemical or pharmacological effects on these enzymes the circadian viriations have to be considered by measuring at different times of day (e.g. fat diet); for only the area of enzyme activit

Alcohol Oxidoreductases↗

PubMed1976

[Hypertension and bilateral stenosis of the renal artery associated with congenital hypoplasia of the intrahepatic bile ducts (author's transl)].

Report of a 10-year-old boy with congenital hypoplasia of the intrahepatic bile ducts, the socalled MacMahon-Thannhauser-Syndrome. The patient had been suffering from a varying degree of jaundice since his 2nd day of life and from pruritus since his 21st month of life. Furthermore, he had hepatomegaly, a systolic cardiac murmur, hypogenitalism, retarded growth, and finally hypertension. Transitory xanthomas existed between 1 3/4 and 2 3/4 years of age. Signs of persistent intrahepatic cholestasis was manifested by increased levels of bilirubin and bile acids in serum as well as raised activities of leucine aminopeptidase, gamma-glutamyl transpeptidase and alkaline phosphatase. Pathological values of serum glutamic dehydrogenase pointed to a persistent destruction of liver cells. Without treatment, the activities of vitamin K dependent clotting factors were decreased. Cholesterol, phosphatides and triglycerides in serum were increased and lipoprotein-X was detectable. Aortography revealed stenosis of both renal arteries. An exploratory laparotomy and 5 liver biopsies led to the diagnosis of hypoplasia of the intrahepatic bile ducts. Therapeutic trials with steroids and the anion exchange resin "cholestyramine" were ineffective. Phenobarbital relieved the pruritus. Parenteral administration of fat soluble vitamins restored the activity of vitamin K dependent clotting factors to normal. The high blood pressure fell significantly due to treatment with adelphan. The etiology of hypoplasia of the intrahepatic bile ducts is unknown. It may be a malformation or an obliteration secondary to inflammation. In our patient, narrowing of the renal arteries, increase of plasma-renin activity and hypertension were probably secondary to hyperlipidemia. It has been suggested that hyperlipemia secondary to cholestasis may be due to a disturbance of lipoprotein metabolism. A review of reports on 118 patients suffering from intrahepatic bile ducts hypoplasia is included.

Bile Ducts, Intrahepatic↗

PubMed1995

Changes in serum lipoprotein(a) in hyperlipidemic subjects undergoing long-term treatment with lipid-lowering drugs.

Though the exact physiology and pathology of lipoprotein(a) [Lp(a)] remains unknown, it has been demonstrated that increased serum Lp(a) levels are correlated with an increased risk of atherosclerotic vascular disease. The effects of lipid-lowering drugs on Lp(a) levels is unclear because of inconsistencies between study designs. This study analyzes the effects of the commonly used lipid-lowering drugs pravastatin (PRAV), lovastatin (LOV), and cholestyramine (CHOL) on serum Lp(a) and other serum lipid levels in a parallel study design. Hyperlipidemic men (n = 32) were enrolled from three centers and treated for 48 weeks in a multicenter clinical trial using PRAV, LOV, CHOL, or a placebo (for the first 16 weeks only). Baseline serum low-density lipoproteins (LDL-C), high-density lipoproteins (HDL-C), and triglycerides were 199 +/- 38, 40 +/- 9, and 160 +/- 70 mg/dl, respectively. At the end of 48 weeks, serum plasma LDL-C declined in patients randomized to PRAV, LOV, and CHOL, respectively, by 31%, 29%, and 23% (all p < 0.001); HDL increased by 4%, 11%, and 11% (all p < 0.001); and TG changed by -16%, -28%, and +43% (all p < 0.001). Subjects in PRAV and LOV changed Lp(a) by 9% and 3%, respectively. Although there was an initial Lp(a) decline in the first 8 weeks of CHOL therapy (p < 0.05, ANOVA), this returned to baseline after 48 weeks. In this parallel study design PRAV, LOV, and CHOL are effective LDL-lowering medications with minimal effects on plasma Lp(a).

Adult↗

PubMed1987

In vitro labeling of peroxisomal cholesterol with radioactive precursors.

Peroxisomes isolated from rat liver were incubated with [3H]squalene and [3H]mevalonate and the subsequent incorporation of radioactivity into cholesterol studied. The isolated lipids became labeled after incubation with both precursors. In contrast to findings with microsomes, trypsin and detergent treatment of peroxisomes did not influence the rate of cholesterol synthesis. In addition, the luminal content of peroxisomes could alone mediate this synthetic process. Upon treatment of rats with various inducers of peroxisomes and of the endoplasmic reticulum, as well as upon feeding with cholesterol and cholestyramine, large differences in the pattern of in vitro incorporation of [3H]mevalonate into the cholesterol of peroxisomes and microsomes were observed. Injection of this precursor also resulted in high initial labeling of peroxisomal cholesterol in vivo. These experiments indicate that cholesterol synthesis may also occur in peroxisomes.

Animals↗

PubMed1997

Comparison technetium of Tc-99m disofenin cholescintigraphy with ultrasonography in the differentiation of biliary atresia from other forms of neonatal jaundice.

Technetium Tc-99m disofenin cholescintigraphy (CS) and ultrasonography (US) are two major clinical methods used in differentiating biliary atresia (BA) from neonatal jaundice. To compare the diagnostic utility of these two modalities, 66 patients with neonatal cholestasis (15 BA, 3 choledochal cyst (CC), 32 neonatal hepatitis, 13 prolonged jaundice, 2 total parenteral nutrition, and 1 sepsis) underwent Tc-99m disofenin CS and US. The diagnostic sensitivity, specificity, and accuracy of CS in differentiating BA from other forms of neonatal jaundice was 100%, 87.5%, and 90.5%, respectively, and for US 86.7%, 77.1%, and 79.4%, respectively. Tc-99m disofenin CS after premedication with phenobarbital and cholestyramine is a convenient and reliable method of differentiating BA from neonatal hepatitis, with a diagnostic accuracy superior to that of US. However, US is the initial imaging procedure of choice in patients presenting with jaundice to rule out anatomic anomalies such as CC.

Biliary Atresia↗

PubMed1984

In vitro adsorption of bile salts and aspirin to sucralfate.

Sucralfate, an aluminum salt of sulfated sucrose, is a new drug designed for the treatment of peptic ulcer. Sucralfate has been reported to be useful in a variety of situations including prevention of aspirin-induced gastric mucosal damage. We investigated the in vitro adsorption of bile salts or aspirin to sucralfate in environments simulating the stomach (pH 1.5), small intestine (pH 7), and colon (pH 7.8). Bile salts were incubated with sucralfate, and the quantity of bile salt adsorbed was calculated by subtraction from the amount remaining in solution after centrifugation at 12,500g for 30 min. Adsorption experiments were performed in bile salt solutions at pH 1.5 and 7.0 with 0-10 g/dl sucralfate using glycocholate, glycochenodeoxycholate, taurocholate, taurodeoxycholate, or taurochenodeoxycholate. The dihydroxy-unconjugated bile salts, deoxycholic, and chenodeoxycholic salts were tested at pH 7.8. Binding capacity (micromoles per gram sucralfate) was calculated from the linear regression of micromoles bound vs grams sucralfate incubated. Sucralfate adsorbed all bile salts tested (except taurocholic acid at pH 1.5) but was less effective than cholestyramine. Sucralfate does not adsorb sufficient bile salts at neutral pH to cause bile salt depletion. Aspirin was minimally adsorbed by sucralfate [7.5 mumol (1.4 mg)/g sucralfate, pH 1.5], and thus adsorption of aspirin does not explain the protective effect of sucralfate against aspirin injury.

Adsorption↗

PubMed1982

Semipurified dietary fiber and small-bowel morphology in rats.

Newly weaned rats fed 12 weeks on a diet containing no dietary fiber or no fiber except for 10% cellulose, maintained the leaf-like intestinal villous morphology present at weaning, as observed by scanning electron microscopy. In rats on a normal laboratory diet the jejunal morphology showed progression from the leaf-like villous pattern at weaning to broad-leafed, long-ridged villi of adulthood. Pectin added to a no-fiber diet caused structural changes similar to but less well developed than those changes in the rats on a standard diet. Striking differences were noted not only in the appearance of the intestinal villi but in the number of villi per square centimeter between those animals on no fiber or no fiber except cellulose and those animals on pectin or standard diets. Cholestyramine, a strong pharmacological bile salt-binding agent, when added to a no-fiber diet, did not promote development of the usual villous pattern, and the structure remained the same as that in rats on no-fiber and cellulose diets. Cellulose (no bile salt-binding capability) and pectin (weak bile salt-binding capability) added to a no-fiber diet were associated with significant differences in the number of villi in both the jejunum and the ileum. The observed changes in morphology are unlikely to be due to differing bile salt-binding capabilities of different fiber substances.

Animals↗

PubMed1978

Dieldrin-14C elimination from turkeys.

A series of experiments were conducted to find ways of removing dieldrin2 residues from tissues of broiler-type turkeys (Meleagris gallopavo). The turkeys were contaminated with dieldrin and dieldrin-14C by oral dosing. Elimination was measured by assaying for 14C in the droppings. Carcass retention was measured by assaying the tissue for 14C, and in one experiment, dieldrin residues were measured by electron capture gas-liquid chromatography. Charcoal, Colestipol, and cholestyramine at dosages approximately equal to an intake of 5% of the diet were ineffective gastrointestinal adsorbants for removing dieldrin residues from the turkeys. Starvation accelerated the elimination of dieldrin from the turkeys, but only if the body lipids were reduced to approximately 10% or less of the carcass dry matter.

Aging↗

PubMed1978

Dieldrin-14C elimination from chickens.

A series of experiments was conducted with chickens contaminated with dieldrin-14C to find ways of accelerating the elimination of dieldrin from their bodies. The results of these experiments indicated that charcoal, imbiber beads, and the anion exchanges resins, Dowex XFS-4022 and Dowex SBR-C1, would not be useful agents for increasing the amount of dieldrin eliminated via feces (droppings) of chickens. Further, imbiber beads coalesced in the gizzard of the chickens and reduced their appetites. The anion exchange resin, cholestyramine, might be useful as gastrointestinal absorbant for increasing dieldrin elimination in chickens because it increased carbon-14 elimination in droppings, but its effect on carbon-14 residues in carcasses was not clear. We elected not to investigate this compound further. Probucol, investigated because it might alter gastrointestinal absorption or blood physiology that would affect dieldrin elimination, did not increase dieldrin elimination. Severe starvation was the only method investigated that clearly was useful for increasing dieldrin elimination because it increased carbon-14 elimination in droppings and reduced carbon-14 residues in carcasses.

Animals↗

PubMed1980

Secondary regulatory sites in rat liver cholesterol biosynthesis: role of 5-pyrophosphomevalonate decarboxylase.

The activity of 5-pyrophosphomevalonate decarboxylase in 43,000 g supernatant fractions from livers and kidneys of male adult rats has been determined. Enzyme activity in liver is significantly increased when rats are fed a diet containing 3% cholestyramine (268% of control rats) and decreased when fed a diet containing 2% cholesterol (25% of control rats). No circadian rhythm of enzyme activity is found in liver or kidneys. These results show that variations in hepatic cholesterogenesis affect the activity of 5-pyrophosphomevalonate decarboxylase in a similar way as other enzymes involved in the biosynthesis of cholesterol.

Animals↗