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PubMed1989

[Drug treatment of hyperlipidemia].

In the therapy of hyperlipemia nicotinic acid derivates, cholestyramine, fibrate derivates and HMG-CoA-reductase inhibitors are drugs of choice. The most important drugs of each group, the mode of action and the side effects are presented. In the therapy of hypercholesterolemia HMG-CoA-reductase inhibitors alone or in special cases in combination with low dose of cholestyramine are best qualified. For the treatment of hypercholesterolemia and hypercholesterolemia fibrate derivates are recommended.

Cholesterol, HDL↗

PubMed1989

A pilot study on intensive lipid lowering--a new approach to cardiac rehabilitation.

The deleterious effects of raised plasma lipids on the progression of coronary artery disease has been well established. Recent research data suggests that intensive lipid lowering represents a new approach to Cardiac Rehabilitation. There was a total of twenty-four participants with twenty-one (87.5%) males and three (12.5%) females. There were seventeen Chinese (70.8%), six Indians (25%) and one Malay (4.2%). Their ages ranged from group forty to forty-nine, five participants (20%); fifty to fifty-nine, twelve participants (50%); sixty to sixty-nine, six participants (25%) and seventy to seventy-nine, one participant (5%). In this study, twelve individuals were treated with Cholestyramine, seven by Gemfibrozil, four by Clofibrate and three by Bezafibrate. The duration of antilipid treatment ranged from two to eighteen months (mean eight months). Side effects were reported in twelve patients (50%) on Cholestyramine who complained of constipation while one (4%) on Bezafibrate had abnormal liver function tests (raised SGOT and SGPT). All patients had been on an exercise and diet control program for one year which they were enrolled in an intensive lipid-lowering protocol. The pre and post treatment lipid profiles with lipid-lowering agents showed 18% reduction for Triglycerides, 15% reduction for Total Cholesterol, 5% increase for HDL-Cholesterol, 19% decrease in LDL Cholesterol, 19% decrease in Total Cholesterol: HDL ratios. The initial results suggest that an intensive lipid-lowering strategy in a Cardiac Rehabilitation Program appears to have a beneficial effect on lipid profiles and represents an expanded approach to lipid management involving exercise, nutrition and pharmacological intervention.

Adult↗

PubMedDate not supplied

[Relation between the rate of ubiquinone biosynthesis and the activity of cholesterogenesis in the rat liver and kidney].

Incorporation of I-14C-acetate into ubiquinone and sterols was studied in liver and kidney tissues of rats after intragastric administration of cholesterol as well as in the animals kept within 2 days on a diet containing cholestyramine or after the bile duct ligation. The rate of incorporation of the labelled compounds into liver sterols was distinctly decreased within the night under the influence of cholesterol-containing diet, while the higher rate of incorporation of the labelled compounds was found in liver tissue of rats, treated with cholestyramine or after bile duct ligation as well as in control animals during night. Regression-correlation analysis demonstrated the positive linear correlation between rates of incorporation of the labelled compounds into ubiquinone and sterols in liver tissue of all the rat group studied. The corresponding correlation was less distinct in kidney tissue.

Animals↗

PubMed1985

Rates of low density lipoprotein uptake and cholesterol synthesis are regulated independently in the liver.

The relationship between rates of hepatic sterol synthesis and rates of hepatic low density lipoprotein (LDL) uptake (clearance) was studied in animals with high (rats), low (female hamsters), and very low (male hamsters) basal rates of hepatic sterol synthesis. In rats and female hamsters, rates of hepatic sterol synthesis were varied over a 110-fold range by feeding cholesterol or cholestyramine; nevertheless, rates of hepatic LDL clearance remained essentially unchanged as did plasma LDL-cholesterol concentrations. In contrast, in male hamsters, which have a very limited capacity to synthesize cholesterol in the liver, cholestyramine feeding increased rates of hepatic LDL uptake by 2.5-fold and this was associated with a 50% reduction in plasma LDL-cholesterol concentrations. The observed increase in LDL uptake was due to an increase in receptor-dependent LDL transport while receptor-independent lipoprotein uptake remained constant. These studies suggest that rates of hepatic cholesterol synthesis and receptor-dependent LDL uptake are regulated independently. Furthermore, the primary response of the liver to changes in cholesterol availability is regulation of sterol synthesis and only when the capacity of this compensatory mechanism is exceeded is the rate of LDL transport altered.

Animals↗

PubMed1979

Effect of diosgenin on lipid metabolism in rats.

The purpose of this study was to determine whether diosgenin suppresses cholesterol absorption in rats, and to examine relevant changes in cholesterol and bile acid metabolism. Diosgenin fed with the diet for 1 week inhibited cholesterol absorption as determined by the serum isotope ratio technique, as well as by measuring in the feces the amount of unabsorbed radioactivity from orally administered [3H]cholesterol. In addition, diosgenin suppressed the serum and liver uptake of radioactivity from co-administered [3H]cholesterol as well as the accumulation of liver cholesterol in the cholesterol-fed rat; diosgenin was substantially more active than cholestyramine or beta-sitosterol. In vitro, diosgenin had no effect on the activity of rat pancreatic esterase. Diosgenin decreased the elevated cholesterol in serum LDL and elevated cholesterol in the HDL fraction of cholesterol-fed rats; diosgenin had no effect on serum cholesterol in normocholesterolemic rats. In contrast to cholestyramine, diosgenin markedly increased neutral sterol excretion without altering bile acid excretion; in vitro, diosgenin had no effect on bile acid binding. Diosgenin treatment increased hepatic and intestinal cholesterol synthesis as well as the activity of hepatic HMG CoA reductase. This was accompanied by increased biliary concentration of cholesterol, but not of bile acids. Diosgenin had no effect on cholesterol synthesis when added to normal rat liver homogenates. It was concluded that diosgenin interferes with the absorption of cholesterol of both exogenous and endogenous origin; such interference is accompanied by derepressed, i.e., increased, rates of hepatic and intestinal cholesterol synthesis. The increased unabsorbed cholesterol together with enhanced secretion of cholesterol into bile resulted in increased excretion of neutral sterols without affecting the biliary and fecal excretion of bile acids.

Acetates↗

PubMed1979

Measurement of cholic acid synthesis and secretion by isolated rat hepatocytes.

Liver cells isolated from normal and cholestyramine-treated rats were incubated as cell suspensions for up to 4 hr in a simple, defined medium. The bile acid concentration in cells plus cell medium was determined by gas-liquid chromatography. Normal hepatocytes synthesized cholic acid at an initial rate of 0.25 nmol/mg cell protein per hr, which is comparable to rates reported from in vivo methods. This rate was increased more than 4-fold when rats were fed a cholestyramine-containing diet for 7 days prior to liver cell isolation. Although cholic acid was secreted into the cell medium during the incubation, it could not be assayed reliably by the hydroxysteroid dehydrogenase assay method, contrary to the reports of Anwer et al. 1975. Biochem. Biophys. Res. Commun. 64: 603 and Gardner and Chenouda 1978. J. Lipid Res. 19: 985.

Animals↗

PubMed1977

Bile acids in serum and bile of infants with cholestatic syndromes.

The concentration of individual bile acids in serum was measured in 18 neonates and infants with various cholestatic conditions (extrahepatic biliary atresia, neonatal hepatitis syndrome, chronic intrahepatic cholestasis and posthemolytic cholestasis). The cholate/chenodeoxycholate ratio in serum was smaller than one in all patients with neonatal hepatitis syndrome or extrahepatic biliary atresia, cholestatic conditions which were accompanied by signs of liver cell injury. It was greater than one in the patients with chronic intrahepatic cholestasis. Administration of cholestyramine to patients with patent extrahepatic bile ducts decreased the total concentration bile acids in serum and elevated the cholate/chenodeoxycholate ratio. Thus, cholestyramine administration may be of diagnostic value for evaluation of bile duct patency in cholestasis of infancy. Differences between the bile acid pattern in serum and bile were observed. Thus, the cholate/chenodeoxycholate ratio was always higher in bile than in serum. 3beta-hydroxy-5-cholenoic acid found in serum was not detectable in bile. This finding suggests that impairment of biliary excretion rather than increased hepatic synthesis is responsible for elevation of this monohydroxy bile acid in serum.

Bile↗

PubMed1983

Regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase and its mRNA in rat liver as studied with a monoclonal antibody and a cDNA probe.

A monoclonal antibody directed against 3-hydroxy-3-methylglutaryl Coenzyme A reductase and a cDNA to reductase mRNA were used to study the subunit structure of the enzyme and the regulation of its mRNA in rat liver. Although the monoclonal antibody and the cDNA were made with materials from cultured hamster cells, the two reagents cross-reacted with reductase protein and mRNA from rat liver. By sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting with monoclonal antibody, the subunit molecular weight of rat liver reductase was 90,000. When the enzyme was solubilized from microsomes by freeze-thawing, the subunit molecular weight was reduced to 52,000-58,000, owing to proteolysis. This proteolysis was inhibited by EGTA and leupeptin. The cDNA probe for reductase, radiolabeled with 32P, hybridized to restriction fragments of genomic DNA from rat liver, as visualized by Southern blot analysis. In the livers of control rats, no reductase mRNA was detected when the 32P-cDNA was blot-hybridized to poly(A+) RNA. Hepatic reductase activity was increased 45-fold when rats were fed cholestyramine and mevinolin. Under these conditions, the amount of immunodetectable reductase protein rose by 33-fold, and the reductase mRNA became visible by blot hybridization as a band of approximately 4 kilobases in length. When the mevinolin/cholestyramine-treated rats were fed cholesterol, reductase activity and immunodetectable protein declined markedly and the reductase mRNA was reduced to barely detectable levels. We conclude that treatment with cholestyramine and mevinolin increases the amount of reductase protein in rat liver by elevating the amount of its mRNA and that cholesterol feeding to such induced rats lowers the amount of hepatic reductase protein by decreasing the level of its mRNA.

Animals↗

PubMed1982

Hydroxylations in biosynthesis of bile acids. Isolation of subfractions with different substrate specificity from cytochrome P-450LM4.

Chromatography of electrophoretically homogeneous cytochrome P-450LM4 from cholestyramine-treated rabbits on octylamine-Sepharose resulted in the isolation of two subfractions, cytochrome P-450LM4 I and cytochrome P-450LM4 II, with different catalytic properties. The original cytochrome P-450LM4 fraction catalyzed 7 alpha-hydroxylation of cholesterol, 12 alpha-hydroxylation of 5 beta-cholestane-3 alpha, 7 alpha-diol, 25-hydroxylation of 5 beta-cholestane-3 alpha, 7 alpha-diol and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol, 6 beta-hydroxylation of testosterone, and demethylation of ethylmorphine. Cytochrome P-450LM4 I was inactive in cholesterol 7 alpha-hydroxylation, but catalyzed the other hydroxylations. Cytochrome P-450LM4 II catalyzed efficient cholesterol 7 alpha-hydroxylation. It also catalyzed the other hydroxylations, although at lower rates than cytochrome P-450LM4 I. Emulgen inhibited all steroid hydroxylase activities in cytochrome P-450LM4 II except the cholesterol 7 alpha-hydroxylase activity. Cytochrome P-450LM4 I and cytochrome P-450LM4 II showed the same apparent molecular weight and spectral properties as the original cytochrome P-450LM4 fraction. The two subfractions differed in amino acid composition. They produced similar but not identical one-dimensional peptide maps upon limited proteolysis with papain, chymotrypsin, and trypsin. The results show that cytochrome P-450LM4 from cholestyramine-treated rabbits contains at least two species with different amino acid compositions and different substrate specificities toward C27-steroids involved in biosynthesis of bile acids.

Amino Acids↗

PubMed1993

Measurement of total hepatic low density lipoprotein receptor levels in the hamster.

The ability to measure the total concentration of low density lipoprotein (LDL) receptors in hepatic tissues is of crucial importance to understanding changes in hepatic cholesterol metabolism. Such measurements can be made in conjunction with estimates of LDL receptor transcriptional activity, cell surface LDL receptor number, and rates of hepatic LDL uptake to evaluate the mechanisms controlling cellular LDL receptor expression. Current methods for assessing hepatic LDL receptor levels use microsomes as a source of LDL receptor, and thus rely on consistent contamination of the microsomal preparation with LDL receptor-containing plasma membranes, endocytic vesicles, and/or secretory vesicles. Because this contamination is variable, and may vary with alterations in either the distribution of LDL receptors among the various cellular membrane fractions or in the composition of the intracellular membranes, measurement of LDL receptor concentration in microsomal fractions may not accurately reflect the total compliment of LDL receptors within the cell. We have developed the methodology for isolating the full complement of hepatic LDL receptor containing membranes by discontinuous sucrose density gradient centrifugation, and for quantitating LDL receptor concentration using a Western immunoblotting procedure that uses an anti-C-terminal LDL receptor peptide polyclonal antiserum and assesses the intensity of color formation by reflectance densitometry. Using this methodology, we observed a 126 kDa immunoreactive band for the bovine adrenal cortex LDL receptor that also exhibited LDL binding activity as visualized by biotinylated LDL-ligand blotting, and a doublet of 140 kDa for the hamster liver LDL receptor. These bands were not observed when ligand blotting was conducted in the presence of either 10 mM EDTA or a 5-fold excess of unlabeled LDL, or when immunoblotting was conducted using either preimmune serum or antiserum that had been preabsorbed with LDL receptor peptide. The intensity of color formation was a linear function of the amount of membrane extract separated by electrophoresis. Intra-assay variation averaged 7%, and inter-animal variation averaged 20%. Cholestyramine, tiqueside, CP-88488, 17 alpha-ethinyl estradiol, mevinolin, and the combination of cholestyramine plus mevinolin, pharmacological interventions known to increase LDL receptor activity in experimental animals, produced the predicted increases in hamster total hepatic LDL receptor concentration that were highly correlated with concomitant increases in HMG-CoA reductase activity and reductions in serum cholesterol.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗

PubMed1996

Development and pharmacology of fluvastatin.

Fluvastatin is the first synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitor to be approved for clinical use, and has been studied extensively in humans since 1986. It is structurally distinct from the other currently available HMGCoA reductase inhibitors (lovastatin, simvastatin, and pravastatin), leading to unique biopharmaceutical properties relative to the other agents of this class. Absorption of fluvastatin is virtually complete across all species, including man, and is not affected by the presence of food. Systemic exposure is limited, as fluvastatin is subject to first-pass metabolism, and the plasma half-life of the drug is approximately 30 minutes. Some 95% of a single dosage of fluvastatin is excreted via the biliary route, with less than 2% of this being the parent compound. Additionally, there is no evidence of circulating active metabolites or accumulation during chronic dosing. Studies of the effect of food on the pharmacokinetics of fluvastatin have demonstrated marked reductions in the rate of bioavailability--from 40% to 60%; however, a comparison of fluvastatin administration with the evening meal or at bedtime has revealed no significant differences in the extent of bioavailability (area under the curve) of these two regimens. Furthermore, no significant difference in pharmacodynamic effect (reduction in low-density lipoprotein cholesterol levels) could be ascertained between mealtime dosing and bedtime dosing. The pharmacokinetics of fluvastatin have also been assessed in various demographic groups. Relative to the general population, plasma concentrations of fluvastatin do not vary as a function of either age or gender. In addition, administration to a patient population with hepatic insufficiency resulted in a 2.5-fold increase in both the rate and extent of bioavailability relative to controls. Also, although minimal alterations of fluvastatin clearance in patients with renal insufficiency are anticipated due to limited renal excretion (5%), a study in this patient group is currently underway to examine this further. Interaction studies have been performed with fluvastatin and several drugs with which it might be coadministered. Cholestyramine, an anionic-binding resin, has a considerable effect in lowering the rate and extent of fluvastatin bioavailability. Although this effect was noted even when cholestyramine was given 4 hours prior to fluvastatin, this regimen did not result in diminished efficacy. Further, no effects on either warfarin levels or prothrombin times were observed in a study involving concomitant administration of warfarin and fluvastatin. Moreover, additional interaction studies with niacin and propranolol have not demonstrated any effect on fluvastatin plasma levels, and administration to a patient population chronically receiving digoxin resulted in no difference in the extent of bioavailability of digoxin relative to control data. The results generated to date in clinical pharmacokinetic studies with fluvastatin thus support its use in a broad population of hypercholesterolaemic patients.

Adult↗

PubMed1975

Massive small bowel resection in a neonate. Four-year follow-up.

All but 17 cm of small intestine was removed in the neonatal period from a child now aged 4 years. Satisfactory growth was achieved by 2 years of age without prolonged intravenous hyper-alimentation. On return to his home environment progress was not maintained, and by 4 years of age, mental and physical retardation were found. Cholestyramine resin was beneficial in reducing stool bulk but had no substantial effect on fat absorption. Compensatory changes in the remaining bowel are recorded.

Body Weight↗

PubMed1994

Serum carotenoids and coronary heart disease. The Lipid Research Clinics Coronary Primary Prevention Trial and Follow-up Study.

OBJECTIVE: To examine the relationship between total serum carotenoid levels and the risk of subsequent coronary heart disease (CHD) events. DESIGN: New analysis of a cohort from the Lipid Research Clinics Coronary Primary Prevention Trial and Follow-up Study (LRC-CPPT). The LRC-CPPT was a multicenter placebo-controlled trial of cholestyramine resin and CHD with a follow-up period of 13 years. Serum carotenoids were measured at baseline. PARTICIPANTS: The placebo group of the LRC-CPPT, which consisted of 1899 men aged 40 to 59 years with type II-a hyperlipidemia and without known preexisting CHD, cancer, or other major illnesses. MAIN OUTCOME MEASURES: Nonfatal myocardial infarctions and deaths attributable to CHD ascertained from hospital records, autopsy reports, and death certificates and reviewed by a panel of cardiologists. RESULTS: After adjustment for known CHD risk factors including smoking, serum carotenoids were inversely related to CHD events. Men in the highest quartile of serum carotenoids had an adjusted relative risk (RR) of 0.64 (95% confidence interval [CI], 0.44 to 0.92) compared with the lowest quartile. For men who never smoked, this RR was 0.28 (95% CI, 0.11 to 0.73). CONCLUSIONS: The LRC-CPPT participants with higher serum carotenoid levels had a decreased risk of incident CHD. This finding was stronger among men who never smoked.

Adult↗

PubMed1998

Persistence of use of lipid-lowering medications: a cross-national study.

CONTEXT: Although clinical trials have demonstrated the benefits of lipid-lowering therapy, little is known about how these drugs are prescribed or used in the general population. OBJECTIVE: To estimate predictors of persistence with therapy for lipid-lowering drug regimens in typical populations of patients in the United States and Canada. DESIGN: A cohort study defining all prescriptions filled for lipid-lowering drugs during 1 year, as well as patients' demographic and clinical characteristics. SETTING: New Jersey's Medicaid and Pharmacy Assistance for the Aged and Disabled programs and Quebec's provincial medical care program. PATIENTS: All continuously enrolled patients older than 65 years who filled 1 or more prescriptions for lipid-lowering drugs (N = 5611 in the US programs, and N = 1676 drawn from a 10% sample in Quebec). MAIN OUTCOME MEASURES: Proportion of days during the study year for which patients had filled prescriptions for lipid-lowering drugs; predictors of good vs poor persistence with therapy. RESULTS: In both populations, patients failed to fill prescriptions for lipid-lowering drugs for about 40% of the study year. Persistence rates with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors were significantly higher than those seen with cholestyramine (64.3% vs 36.6% of days with drug available, respectively). Patients with hypertension, diabetes, or coronary artery disease had significantly higher rates of persistence with lipid-lowering regimens. In New Jersey, multivariable analysis indicated that the poorest patients (those enrolled in Medicaid) had lower rates of drug use than less indigent patients (those enrolled in Pharmacy Assistance for the Aged and Disabled) after adjusting for possible confounders, despite virtually complete drug coverage in both programs. When rates of use were measured in the US population for the 5 years following the study year, only 52% of surviving patients who were initially prescribed lipid-lowering drugs were still filling prescriptions for this drug class. CONCLUSION: In all populations studied, patients who were prescribed lipid-lowering drug regimens remained without filled prescriptions for over a third of the study year on average. Rates of persistence varied substantially with choice of agent prescribed, comorbidity, and socioeconomic status, despite universal coverage of prescription drug costs. After 5 years, about half of the surviving original cohort in the United States had stopped using lipid-lowering therapy altogether.

Aged↗

PubMed1990

Bile acid sequestrants.

The bile acid sequestrants, cholestyramine and colestipol, are the drugs of choice for the treatment of patients with hypercholesterolemia caused by increases in LDL-cholesterol levels without concurrent hypertriglyceridemia (type IIA and type IIB hyperlipoproteinemia). Longitudinal clinical studies with these drugs have shown their ability to slow the progression of atherosclerosis and to limit the consequences of the disease. Bile acid sequestrants can be used with other lipid-lowering drugs such as nicotinic acid or HMG CoA reductase inhibitors, to maximize the cholesterol-lowering effects. The side effect profile of the bile acid sequestrants is tolerable, with most complaints related to effects on the gastrointestinal tract and the bulkiness of the resins.

Chemical Phenomena↗

PubMed1994

Disposition of lorazepam in Gilbert's syndrome: effects of fasting, feeding, and enterohepatic circulation.

The effects of fasting and feeding of a high-carbohydrate, low-fat diet on the glucuronidation and enterohepatic circulation (EHC) of lorazepam were examined in seven healthy men (age 18-30 years) and seven matched patients with Gilbert's syndrome. A simultaneous intravenous/oral dosing regimen was used, with half of each group receiving treatment with neomycin and cholestyramine (neo/chol) to block the EHC of the drug. Feeding increased the clearance of free lorazepam from 10.96 +/- 0.56 (mean +/- SD) to 14.11 +/- 1.21 mL/min/kg (P = 0.05) in patients with Gilbert's syndrome when examined in the presence of neo/chol. Clearances, on the other hand, decreased with feeding in control Gilbert's patients (7.61 +/- 0.54 versus 8.82 +/- 0.48 mL/min/kg), although the differences were not significant (P = 0.09). In contrast to both of these groups, feeding decreased lorazepam clearances (13.33 +/- 0.32 to 12.45 +/- 0.52 mL/min/kg, P = 0.17) in neo/chol-treated normals and increased clearances (9.95 +/- 1.84 to 12.38 +/- 2.05 mL/min/kg, P = 0.04) in control normals. Lorazepam clearances were also 20-40% lower in patients with Gilbert's syndrome compared with normals when studied fasting and with neo/chol, or fed and in the control state (P < 0.05 for both). Thus, the glucuronidation and EHC of lorazepam is sensitive both to diet and to the presence or absence of the Gilbert's trait.

Adolescent↗

PubMed2001

Bile acid sequestrants based on cationic dextran hydrogel microspheres. 2. Influence of the length of alkyl substituents at the amino groups of the sorbents on the sorption of bile salts.

Cationic dextran hydrogel microspheres with pendant quaternary ammonium groups having alkyl substituents (C(2)-C(12)) at quaternary nitrogen were synthesized. The in vitro sorption of sodium salts of four bile acids (glycocholic, cholic, taurocholic, and deoxycholic acids) with these hydrogels was studied as a function of substituent alkyl chain length and bile acid hydrophobicity. Sorption experiments were performed in phosphate buffer solutions (pH 7.4) containing one bile salt (individual sorption) or mixtures of several bile salts (competitive sorption). Parameters for individual sorption were calculated taking into consideration the stoichiometric and cooperative binding of bile salts to oppositely charged polymer hydrogels. The results show that the increase in the length of the alkyl chain of the substituent leads to an increase in both ionization constant K(0) and overall stability constant of binding K, but decreases the cooperativity parameter u. The competitive sorption studies indicate that the hydrogels display a good affinity for both dihydroxylic and trihydroxylic bile salts. The molar ratio of maximum amounts bound for the two types of bile acid is 2 to 1, which is much lower than those reported for other cationic polymers recommended as bile acid sequestrants. The binding constants for the sorption of bile salts by some dextran hydrogels are 20-30 times higher than those obtained for cholestyramine under similar sorption conditions.

Alkylation↗

PubMed1979

Antihypercholesterolemic studies with sterols: beta-sitosterol and stigmasterol.

Stigmasterol, which differs from beta-sitosterol by unsaturation at C22, was tested for antihypercholesterolemic activity under an experimental protocol that gave the results expected with beta-sitosterol and cholestyramine. In terms of serum cholesterol, stigmasterol had a barely significant antihypercholesterolemic effect while exhibiting no obvious effect on the heart or liver. It was concluded that saturation of the side chain, at least at C22, is important in conferring antihypercholesterolemic activity on a sterol.

Animals↗