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At least 19 recordsLinked to original sources
PubMed1975

Evaluation of chromic oxide, glycerol triether, and beta-sitosterol as fecal flow markers in two species of nonhuman primates.

Recovery of beta-sitosterol, glycerol triether (1-hexadecyl-2,3-didodecyl glycerol triether), and chromic oxide was studied in African green monkeys and stumptail macaques consuming diets containing 0.75 mg/Cal cholesterol and 38% of calories as safflower oil or butter. Following oral administration of these compounds, feces were collected daily for 9 days. For all animals, excretion of beta-sitosterol and glycerol triether paralleled one another almost exactly. Except for two animals, this was also true for chromic acid. Essentially 100% of the administered beta-sitosterol and 90-95% of the glycerol triether were recovered; excretion of these markers virtually was complete by day 3. Ninety-two percent of the beta-sitosterol was isolated in the nonsaponifiable lipid extract of the feces with less than 6% in the remaining aqueous phase. A maximum of 3.1% of the beta-sitosterol and 1.8% of the glycerol triether were found in the blood. For stumptail macaques, the major excretory form of beta-sitosterol was the 5 beta-derivative. African green monkeys were more variable; one animal excreted the bulk of the beta-sitosterol unchanged while others excreted greater than 80% as the ring-saturated 5 beta-derivative. Animals consuming the safflower oil containing diet consistently excreted a greater percentage of the beta-sitosterol unchanged, compared with those animals eating the butter containing diet. There was no evidence for steroid ring degradation in any of the animals used in this study.

Animals↗
PubMed1976

Effect of Beta-sitosterol on cholesterol-cholic acid-induced gallstone formation in mice.

Beta-sitosterol has been shown to prevent gallstone formation in mice fed 1.2% cholesterol and 0.5% cholic acid (lithogenic diet). The incidence of gallstone formation in the mouse by the addition of 2.5% sitosterol in the lithogenic diet is about 35.5% in male and 25% in female. The condition of the liver, whether fatty or normal, did not correlate with the presence or absence of cholelithiasis. The serum and liver cholesterol levels of mice fed either sitosterol and cholesterol or sitosterol and cholic acid is lower than those of mice fed cholesterol or cholic acid alone. Elevation of liver phospholipid concentration was noticed in mice fed sitosterol or a combination of sitosterol with cholesterol or cholic acid or both cholesterol and cholic acid.

Animal Feed↗
PubMed1976

Side chain hydroxylation of cholesterol, campesterol and beta-sitosterol in rat liver mitochondria.

The extent of the side chain hydroxylation of cholesterol, campesterol (24 alpha-methylcholesterol), and beta-sitosterol (24 alpha-ethylcholesterol) in rat liver mitochondria has been compared. Two beta-sitosterol metabolites, tentatively identified by liquid chromatography, thin-layer chromatography, gas-liquid chromatography, combined with radioactivity detection, and gas-liquid chromatography-mass spectrometry as the 26- and 29-hydroxy derivatives, were formed in the proportion 1:1. The sum of 26-hydroxy- and 29-hydroxy-beta-sitosterol obtained amounted only to about one-fourth of the yield of 26-hydroxycholesterol. Campersterol appeared to give rise only to 26-hydroxycampesterol (tentatively identified), which was formed in similar yields as 26-hydroxycholesterol (0.2-0.4%). The formation of 29-hydroxy-beta-sitosterol but not of 28-hydroxycampesterol indicates that the omega-hydroxylation of the steroid side chain is dependent on the length of the side chain. Cholesterol gave rise to identifiable amounts of a 25-hydroxy derivative but the formation of 25-hydroxy derivatives of beta-sitosterol and campesterol could not be established with certainty. 24-hydroxycholesterol was also found to be formed in the mitochondrial system. The ratio between the yields of 26- and 25-hydroxychoelsterol ranged between 2 and 3, and that between 26- and 24-hydroxycholesterol was about 10.

Animals↗
PubMed1976

[Sitosterol in familial hyperlipoproteinemia type II. A randomized double-blind cross-over study].

The effect of beta-sitosterol on the lipid and lipoprotein level was evaluated in a randomised double-blind cross-over trial in 24 patients with primary familial type II hyperlipoproteinaemia over a period of 16 weeks. All patients completed the trial, however 10 of them had to be excluded from the evaluation due to fluctuations of their body weight or unreliable drug intake. Sitosterol lowered the total cholesterol level by 12.5% (P less than 0.01) from 9.96 mmol/l (3.69 g/l) to 8.37 mmol/l (3.23 g/l). The LDL-cholesterol level was lowered by 19.5% (P less than 0.05). The sitosterol concentration in plasma was consistently lower than 0.3% of total cholesterol. No side effects or tachyphylaxis was observed in the course of the trial. A return to normal of an increased serum cholesterol level by a combination of a lipid lowering diet and sitosterol monotherapy was only achieved in one patient.

Adolescent↗
PubMed1977

A comparison of hypocholesterolemic activity of beta-sitosterol and beta-sitostanol in rats.

The hypocholesterolemic activity of beta-sitosterol and its hydrogenated product, beta-sitostanol (dihydrositosterol or stigmastanol) has been compared in young male rats. When cholesterol was included in the diet, sitostanol consistently exhibited significantly greater hypocholesterolemic activity than sitosterol. There were no apparent differences in the effects of the sterol and the stanol on the concentration of liver cholesterol and triglyceride. Increases in plasma triglyceride due to feeding sitosterol were not observed with sitostanol. Incorporation of dietary sitostanol into plasma, liver and other tissues was always negligible, and thus this stanol was almost completely recovered in feces, while there was considerable deposition of sitosterol (mean fecal recovery being 85% to 92%). The increase in fecal output of dietary cholesterol was significantly greater with the stanol than with sterol. There was no demonstrable negative effect on growth and weight of major visceral tissues in rats fed the sterol as well as the stanol. These observations together with those reported previously indicate that hydorgenation of phytosterols is a novel approach to enhance their hypocholesterolemic activities without influencing the relative safety of the initial sterols.

Adipose Tissue↗
PubMed1979

Effects of diazacholesterol, triparanol, and beta-sitosterol on egg cholesterol deposition in coturnix quail.

Studies were undertaken to determine the effect of inhibitors of cholesterol synthesis on deposition of cholesterol in eggs of Japanese quail. Results indicate that this bird responds similarly to the laying hen, making it a useful screening device for these types of compounds. Administration of either triparanol or 20,25 diazacholesterol resulted in a decreased cholesterol content of the yolk. Concomitant with this decrease was an increase in desmosterol deposition. Beta sitosterol (2%) fed either alone or with lecithin (2%) did not result in a decrease in egg yolk cholesterol. No beta-sitosterol was found in the egg yolk. Diazacholesterol fed either with sitosterol, or sitosterol plus lecithin, was not effective in reducing the total sterol content of egg.

Administration, Oral↗
PubMed1978

beta-Sitosterol as a nonabsorbable marker of dietary lipid absorption in man.

beta-[14C]Sitosterol was evaluated for its usefulness as a nonabsorbable marker of lipid absorption in intubation studies. A liquid meal, including [3H]triolein as a marker of absorbable lipid, was used. The beta-sitosterol was shown to remain well mixed with triolein in the gastric antrum, validating its suitability for this type of study. In small bowel fluid, the beta-sitosterol was shown to partition into the aqueous phase in proportion to triolein and its hydrolysis products. With this system, lipid absorption was shown to take place chiefly in the jejunum in normal individuals.

Carbon Radioisotopes↗
PubMed1978

Sitosterol in juvenile type II hyperlipoproteinemia.

The effect of beta-sitosterol on plasma lipids and lipoproteins was evaluated in a randomized double-blind cross-over trial in 15 children and adolescents with familial hypercholesterolemia over a period of 6 months. Twelve patients completed the study, with good adherence to drug intake. Sitosterol lowered the plasma total choelsterol by 6%, LDL cholesterol by 7% and HDL cholesterol by 15% (P less than 0.05). This insufficient response of total and LDL cholesterol and the marked fall of HDL cholesterol appears to advise against the use of beta-sitosterol granulate in juvenile type II hyperlipoproteinemia.

Adolescent↗
PubMed1979

Role of 24- and 28-hydroxylated intermediates in the metabolism of beta-sitosterol in the insect Tenebrio molitor.

1. [28-3H]Stigmast-5-ene-3 beta, 28-diol and [23,23,25-3H]stigmast-5-ene-3 beta, 24-diol were synthesized. 2. Each of the samples was mixed with beta-[4-14C]sitosterol and administered to Tenebrio molitor larvae. 3. The former compound is not utilized by the insect; the latter, although metabolized to 24(28)-ethylidene sterols and cholesterol, is not a beta-sitosterol metabolite. 4. The above results are discussed in relation to the mechanism of formation of the 24(28)-double bond in beta-sitosterol metabolism in T. molitor.

Hydroxylation↗
PubMed1978

Fecal beta-sitosterol in patients with diverticular disease of the colon and in vegetarians.

Fecal sterol analysis showed that excretion of beta-sitosterol, a major component of poorly absorbable dietary vegetable sterols, is subnormal in patients with diverticular disease of the colon. Thus, the patients had evidently consumed a diet low in plant materials. The finding agrees with the current opinion that diverticular disease of the colon is associated with dietary fibre deficiency and suggests that fecal beta-sitosterol provides a rough measure of the vegetable intake. In vegetarians the beta-sitosterol excretion was actually high.

Adult↗
PubMed1975

Substrate specificity of lecithin:cholesterol acyltransferase. Esterification of desmosterol, b-sitosterol, and cholecalciferol in human plasma.

Desmosterol and beta-sitosterol were esterified when incubated with normal human plasma. The initial rate of demosterol esterification was 1.7 times faster, and that of beta-sitosterol 0.4 times slower, than the esterification rate of cholesterol. These ratios were found to be almost the same when plasma from different normal individuals was tested. Plasma from a patient with familial lecithin:cholesterol acyltransferase deficiency did not esterify any of the sterols. The esterification of desmosterol and beta-sitosterol was considerably slower in normal plasma in which in vitro cholesterol esterification previously had taken place. The different esterification rates could not be explained by a different affinity of the plasma lipoproteins for the sterols tested. Cholecalciferol added to normal plasma did not become esterified.

Acyltransferases↗
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↗
PubMed1978

The influence of beta-sitosterol on biliary cholesterol saturation and bile acid kinetics in man.

beta-Sitosterol, administered in doses of 12 g/d, resulted in a mean decrease of 11% in serum cholesterol and of 12% in biliary cholesterol saturation after 6-8 weeks. Sustained effects were found in some individuals treated for longer periods. Significant changes in bile acid kinetics could not be detected. The results lend support for further investigations of sitosterol as a possible adjunct therapy in cholelitholytic treatment.

Adult↗
PubMed1978

Bioconversion of sitosterol to useful steroidal intermediates by mutants of Mycobacterium fortuitum.

A series of mutants which are blocked at various stages of the sterol degradative pathway have been isolated from the potent sterol degrader Mycobacterium fortuitum ATCC-6842. Sitosterol bioconversions by these mutants result in the accumulation of a number of intermediate compounds, some of which are potentially useful as substrates in the manufacture of medically important steroids. These intermediates include androst-4-ene-3,17-dione, androsta-1,4-diene,3,17-dione, ring A-degraded tricyclic compounds and various 9alpha-hydroxy-steroids.

Androstadienes↗
PubMed1978

Comparison of absorption and metabolism of beta-sitosterol and beta-sitostanol in rats.

The fates of [4-14C]beta-sitosterol ([14C]S) and [4-14C]beta-sitostanol ([14C]HS) were compared after after oral or intravenous administration to rats. Excretion into feces of oral [14C]HS was significantly higher than that of [14C]S. More than 97% of [14C]HS and 88% of [14CS]S were recovered in the feces within 7 days. Thus, deposition of [14C]HS was negligible in the tissues that were examined. Turnover in serum of [14C]HS which was injected intravenously appeared to be more rapid than that of [14C]S; [14C]HS was excreted as neutral steroids at a rate more than twice that of [14C]S. The rate of excretion of [3H]cholesterol was slightly greater when HS was administered simultaneously. The liver contained significantly less radioactivity after [14C]HS than after [14C]S administration. More [14C]HS than [14C]S was present in esterified form in serum and liver. The ratio of sterol in very low density lipoprotein to that in high density lipoprotein was less for HS or S than for endogenous cholesterol; this was particularly marked with HS. These results suggest that HS would be a more effective hypocholesterolemic agent than S.

Administration, Oral↗