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PubMedDate not supplied

Sluggish sitosterol turnover and hepatic failure to excrete sitosterol into bile cause expansion of body pool of sitosterol in patients with sitosterolemia and xanthomatosis.

Sitosterolemia and xanthomatosis are characterized by the development of tendon and tuberous xanthomas at an early age and premature atherosclerosis despite normal plasma cholesterol concentrations. The reason(s) for the xanthoma formation and premature atherosclerosis are not clearly understood. The accumulation of sitosterol in the tissues of these patients could be due to increased uptake of low density lipoprotein (LDL) via LDL receptors because of an expanded sitosterol pool caused by sluggish turnover and decreased excretion of sitosterol into bile and feces coupled with the hyperabsorption of sitosterol. We have studied sitosterol and cholesterol turnovers, the biliary and fecal excretion of neutral and acidic steroids, and the response of plasma sterol (sitosterol and cholesterol) levels to either a sterol-free formula or low plant sterol diet in three patients. The average half-life of the first exponential (tA1/2) for sitosterol was 9.2 +/- 3.3 (mean +/- SD) days, which was more than twice that in normal humans. The second exponential (tB1/2) was 156 +/- 108 days, which was nearly 10 times longer than that for normal humans. The average cholesterol production rate in pool A was 0.87 g/day, which is about 40% of that in normal humans. Cholesterol synthesis measured by the sterol balance technique was also found to be about 70% lower than that for normal humans. In two patients fed a sterol-free formula diet, by 25 days their plasma sitosterol and cholesterol levels had decreased by 42% and 36%, respectively. However, in one patient plasma sitosterol and cholesterol concentrations remained unchanged while on the low plant sterol-mixed food diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Antihyperglycemic and insulin-releasing effects of beta-sitosterol 3-beta-D-glucoside and its aglycone, beta-sitosterol.

The effect of beta-sitosterol 3-beta-glucoside (antihyperglycemic principle isolated from the aerial part of Centaurea seridis L. var. maritima Lge.) and its aglycone on plasma insulin and glucose levels in normo- and hyperglycemic rats was investigated. The results indicate that oral treatment with the glycoside or with the beta-sitosterol increased the fasting plasma insulin levels. There was a corresponding decrease in fasting glycemia when beta-sitosterol was administered orally. In addition, these compounds improved the oral glucose tolerance test with an increase in glucose-induced insulin secretion. But when these products were administered orally, the effect of glycoside, either on fasting insulinemia or on glucose-induced insulin secretion, lasted longer than that of aglycone. The present study compared these effects with those of glibenclamide. It can be assumed that beta-sitosterol 3-beta-D-glucoside acts by increasing circulating insulin levels, and that this effect is due to their aglycone: beta-sitosterol.

Animals↗
PubMed1970

Metabolism of beta-sitosterol in man.

The metabolism of beta-sitosterol was compared to that of cholesterol in 12 patients. Sterol balance methods were supplemented by radiosterol studies, with the following results. (a) Plasma concentrations of beta-sitosterol ranged from 0.30 to 1.02 mg/100 ml plasma in patients on intakes of beta-sitosterol typical of the American diet. Plasma levels were raised little when intakes were increased greatly, and on fixed intakes they were constant from week to week. On diets devoid of plant sterols, the plasma and feces rapidly became free of beta-sitosterol. (b) The percentage of esterified beta-sitosterol in the plasma was the same as for cholesterol. However, the rate of esterification of beta-sitosterol was slower than that for cholesterol. (c) Specific activity-time curves after simultaneous pulse labeling with beta-sitosterol-(3)H and cholesterol-(14)C conformed to two-pool models. The two exponential half-lives of beta-sitosterol were much shorter than for cholesterol, and pool sizes were much smaller. Values of turnover for beta-sitosterol obtained by the sterol balance method agreed closely with those derived by use of the two-pool model. There was no endogenous synthesis of beta-sitosterol in the patients studied; hence, daily turnover of beta-sitosterol equaled its daily absorption. Absorption of beta-sitosterol was 5% (or less) of daily intake, while cholesterol absorption ranged from 45 to 54% of intake. (d) About 20% of the absorbed beta-sitosterol was converted to cholic and chenodeoxycholic acids. The remainder was excreted in bile as free sterol; this excretion was more rapid than that of cholesterol. (e) The employment of beta-sitosterol as an internal standard to correct for losses of cholesterol in sterol balance studies is further validated by the results presented here.

Adult↗
PubMed1988

Effect of ileal exclusion on lipoprotein sitosterol in familial hypercholesterolaemia.

A plant sterol, sitosterol, was quantitated in very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL) and related to faecal steroids and cholesterol absorption in heterozygous familial hypercholesterolaemia patients with (n = 7) and without ileal bypass (n = 6). The latter had resulted in severe bile acid malabsorption but fractional cholesterol absorption was within low control limits. Serum total and LDL cholesterol and apoprotein B levels were reduced, whereas HDL cholesterol, apoprotein A-I, VLDL and HDL sitosterol concentrations were increased by the ileal exclusion, and the increase in LDL and serum total sitosterol levels was insignificant. In terms of mmol/mol of cholesterol or apoprotein B, however, the LDL and total sitosterol contents were higher in the subjects who had undergone operation. For an unknown reason the sitosterol content increased gradually within the lipoprotein particles from the lighter to the heavier lipoproteins, and the enrichment was similar in the two groups. Dietary sitosterol intake, indicated by faecal sitosterol excretion, was similar in the two groups. The contents of serum total and LDL sitosterol were positively correlated with the dietary sitosterol intake in both groups, and with the fractional cholesterol absorption only in the group not subject to operation. These associations were less consistent for sitosterol contents in other lipoproteins. We conclude that normally the serum sitosterol content reflects cholesterol absorption efficiency even in patients with familial hypercholesterolaemia, provided the dietary sitosterol intake is quite constant. In addition, for unknown reasons ileal exclusion leads to an increased lipoprotein sitosterol content.

Adult↗
PubMed1989

Effect of sitosterol on the rate-limiting enzymes in cholesterol synthesis and degradation.

Attempts were made to develop an animal model for phytosterolemia. Infusion of Intralipid containing 0.2% sitosterol in rats gave circulating levels of sitosterol of about 2.5 mmol/l, which is similar to or higher than those present in patients with untreated phytosterolemia. In addition, the infusions gave serum levels of cholesterol nearly twice those obtained in rats infused with Intralipid alone or Intralipid containing 0.2% cholesterol. The hepatic HMG-CoA reductase activity was unaffected or slightly increased by the sitosterol infusions (not statistically significant). The cholesterol 7 alpha-hydroxylase activity was slightly depressed (ca. 30%). In the case of 7 alpha-hydroxylation of endogenous cholesterol, the depression reached statistical significance (p less than 0.05). The microsomal content of sitosterol in the sitosterol-infused rats was about 30% of that of microsomal cholesterol. The effect of sitosterol on 7 alpha-hydroxylation of cholesterol was investigated by incubations of acetone powder of rat liver microsomes with mixtures of cholesterol and sitosterol. Sitosterol mixed with cholesterol to a composition similar to that found in the above microsomal fraction had a depressing effect on 7 alpha-hydroxylation of cholesterol. This degree of depression was of the same magnitude as that found in the sitosterol infusion experiments. The possibility is discussed that the hypercholesterolemia obtained in the beta-sitosterol-infused rats is due to the inhibitory effect of sitosterol on the cholesterol 7 alpha-hydroxylase.

Animals↗
PubMed1976

Absorption of dietary beta-sitosterol in laying hens and its incorporation into the egg.

Studies were undertaken to determine the dietary beta-sitosterol absorption in laying hens and its incorporation into the egg. Hens were divided into four groups and fed a commercial low-fat laying diet. Group 1 served as controls; the diet of group 2 was supplemented with 10% corn oil; group 3 with 4% plant sterols (emulsion in carboxymethylcellulose); group 4 with 10% corn oil and 4% plant sterols. The daily beta-sitosterol intake of hens in groups 1, 2, 3 and 4 was 0.036 g 0.095 g, 2 g and 2.56 g, respectively. After consuming the diets for 30 to 40 days, cholesterol and beta-sitosterol contents of the eggs were estimated by gas liquid chromatographic and mass spectrometric methods. Feeding corn oil with and without plant sterols increased cholesterol content of the eggs, while feeding plant sterols alone had no effect on egg cholesterol levels. The beta-sitosterol content of eggs from groups 1 and 2 was similar (60-66 mug/g yolk) and feeding plant sterols increased the beta-sitosterol content to a very small extent (82-90 mug/g yolk). Studies on the dietary beta-sitosterol and cholesterol absorption indicated that there was very little absorption of beta-sitosterol. In control hens, beta-sitosterol absorption was about 7% compared to 81% cholesterol absorption. Plant sterols feeding did not affect the beta-sitosterol absorption but reduced cholesterol absorption by 40%. Feeding corn oil alone did not affect cholesterol absorption. Failure to detect any significant amount of beta-sitosterol in these hens. At the peak radioactivity deposition in the eggs, only 2% of the absorbed beta-sitosterol radioactivity was found in the eggs of group 4 compared to 5% found in group 1, while cholesterol radiioactivity was nearly 4 to 5 times in both groups. These data suggested that laying hens synthesized specific lipoproteins for deposition in yolk.

Absorption↗
PubMed1989

Increased sitosterol absorption, decreased removal, and expanded body pools compensate for reduced cholesterol synthesis in sitosterolemia with xanthomatosis.

We measured the turnover and absorption of sitosterol and cholesterol, along with plasma sterol and lipoprotein concentrations, in one control and two subjects with sitosterolemia with xanthomatosis. All individuals consumed the same diet which contained approximately 500 mg/day of cholesterol and 250 mg/day of sitosterol. Sterol absorption was measured by the plasma dual-isotope ratio method and turnover by plasma isotope-kinetic analysis. In two sitosterolemic subjects, 28% and 63% of the sitosterol and 69% and 49% of the cholesterol were absorbed, respectively, compared to 4% of the sitosterol and 44% of the cholesterol in the control. As expected, plasma sitosterol specific activities decayed much more rapidly than cholesterol in the control subject. In contrast, plasma sitosterol and cholesterol specific activity-time curves were similar and decayed more slowly in the sitosterolemic subjects. In the control subject, the total sitotterol pool was 290 mg and was linearly related to low absorption (18 mg/day); whereas the total sitosterol pool was 17 times (4800 mg) and 13 times (3500 mg) larger, respectively, in the sitosterolemic subjects and was expanded out of proportion to increased absorption because of decreased removal. Daily cholesterol turnover and synthesis were markedly reduced in the sitosterolemic subjects. In four sitosterolemic subjects, plasma concentrations of total sterols, low density lipoproteins, and apolipoprotein B were increased, while those of high density lipoproteins and apolipoprotein A-I were low to normal. The low density lipoproteins were very similar to those of normal control subjects in density distribution, peak flotation rate, sterol-to-protein (apolipoprotein B) ratio, particle size, and morphology. These results demonstrate in patients with sitosterolemia with xanthomatosis that: 1) the absorption of sitosterol and cholesterol is enhanced; 2) tissue recognition between cholesterol and sitosterol is lost; 3) total exchangeable sitosterol pools are expanded out of proportion to absorption because of decreased excretion; 4) plasma sterol and lipoprotein concentrations favor tissue deposition; and 5) cholesterol synthesis is diminished. We postulate that the changes in sitosterol metabolism (increased absorption, loss of tissue sterol structural recognition, expanded pools, and hepatic retention) are a response to reduced cholesterol synthesis in these subject.

Absorption↗
PubMed1988

Discrimination between cholesterol and sitosterol for absorption in rats.

The intestinal absorption of cholesterol and sitosterol was compared in rats. The intragastric administration of a single emulsified lipid meal containing either 50 mg of [4-14C]cholesterol or [4-14C]sitosterol resulted in the lymphatic absorption of 18.2% and 0.42% of each sterol, respectively, in 6 hr. This difference was unaltered when the mucosal sterol load was equalized by reducing the cholesterol to 1 mg in the emulsified lipid meal while maintaining the same sitosterol load or when the physical state in the lumen was equalized by infusion of a micellar solution containing both sterols into bile-diverted intestine. Lymphatic cholesterol was 90% esterified compared to 12% for sitosterol. Both sterols were associated predominantly (greater than 70%) with the chylomicron fraction. Eighty percent of the chylomicron cholesterol was recovered as ester with the core lipids, while 77% of the sitosterol was recovered as free sterol with the chylomicron coat. In mucosal homogenates at 6 hr, sitosterol recovery was one-eleventh that of cholesterol. When [3H]cholesterol (10 mg) and [14C]sitosterol (10 mg) were co-administered in an emulsified intragastric lipid meal, sitosterol associated with the brush border isolated 2 hr later was one-fifth that of cholesterol. Similar differences were seen when brush border membranes were incubated in vitro with micellar solutions containing either 50 microM [3H]cholesterol or [14C]sitosterol and the relative uptake of each sterol was unaffected by micellar phospholipid type (egg yolk phospholipids, phosphatidylcholine, or phosphatidylethanolamine).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗
PubMed1969

Absorption and lymphatic transport of cholesterol and sitosterol in the rat.

An attempt was made to determine the mechanism for the greater absorbability of cholesterol as compared to sitosterol. Sitosterol-22,23-(3)H in different combinations with cholesterol-4-(14)C, dissolved in 0.8 ml of triolein, was fed to rats with lymph fistulae. Feeding 1.5, 50, or 100 micro moles of sitosterol resulted in a transfer to the lymph in 24 hr of 3-6% of the sitosterol, largely independent of the dose fed. The total amount of sitosterol transferred to the lymph was therefore almost linearly related to the dose fed. 30% of a tracer dose of cholesterol-4-(14)C fed together with the sitosterol was transferred to the lymph in 24 hr. When a total of 50 micro moles of sterol, containing cholesterol-(14)C and sitosterol-(3)H in the proportions 1:3, 1:1, and 3:1, was similarly fed, we found that sitosterol had no significant effect on the lymphatic transport of the simultaneously fed cholesterol. The ratio of (3)H to (14)C in the lymph was between 0.1 and 0.2 (the ratio in each fed mixture being taken as 1.0). The ratio was constant during the absorption period and independent of the ratio of sterols in the fed sterol mixture. Thus the same percentage of each sterol was always absorbed, and the sterols exerted no mutual interference in each others' absorption. We conclude that the mechanism for specificity in sterol absorption must be located early in the transport of the sterols within the intestinal mucosa cell.

Animals↗
PubMed1983

Some aspects of mechanism of inhibition of cholesterol absorption by beta-sitosterol.

Mixed bile salt micelle solubilized either cholesterol or beta-sitosterol to a comparable extent. When added simultaneously, beta-sitosterol restricted the micellar solubility of cholesterol. beta-Sitosterol also reduced the cholesterol content in the aqueous (micellar) phase of the intestinal contents of rats, the extent of reduction being comparable with that observed in vitro. The intestinal uptake of cholesterol in vivo was equivalent to the micellar incorporation of cholesterol both in vitro and in vivo. beta-Sitosterol had no inhibitory effect on cholesterol absorption from the micellar solution in jejunal loops in situ, whereas the rate of beta-sitosterol uptake was only about one-fifth that of cholesterol. The intestinal uptake of beta-sitosterol intubated into the stomach of rats was about one-fifth that of cholesterol. The intestinal brush-border membrane discriminated these sterols. These results suggest that the restriction of the micellar solubility of cholesterol, rather than the inhibition of uptake from brush-border membrane, is the major determinant for the interference of beta-sitosterol with cholesterol absorption.

Animals↗
PubMed1987

Distribution and partitioning of cholesterol and beta-sitosterol in micellar bile salt solutions.

The distribution of cholesterol and beta-sitosterol in micellar bile salt solutions was studied using an ultrafiltration technique to separate micellar aggregates from monomers present in the intermicellar aqueous phase. The partitioning and the rates of influx across the brush-border membrane of these two sterols from micellar solutions were determined using polyethylene discs and everted jejunal sacs, respectively. Micellar solubilities of cholesterol and beta-sitosterol were not significantly different, whereas the monomer concentration of beta-sitosterol in the intermicellar aqueous phase was significantly lower than that of cholesterol [0.21 +/- 0.02 microM for beta-sitosterol and 25.0 +/- 2.71 (SE) microM for cholesterol, P less than 0.001]. There was no difference in the partitioning nor was there a difference in the rates of influx between cholesterol and beta-sitosterol from micellar solutions containing a similar amount of the two sterols. It is concluded that monomer concentration of beta-sitosterol in the intermicellar aqueous phase is extremely low compared with that of cholesterol, but their partitioning and rates of influx across the membrane are similar. This is primarily attributable to a much higher membrane/monomer partition coefficient of beta-sitosterol than cholesterol and to a direct interaction between micelle and membrane.

Animals↗
PubMed1992

Increased sitosterol absorption is offset by rapid elimination to prevent accumulation in heterozygotes with sitosterolemia.

Using plasma isotope-kinetic methods, we measured the absorption and turnover rates of cholesterol and sitosterol (24-ethylcholesterol) in two obligate heterozygotes (parents) and their homozygous daughter with sitosterolemia with xanthomatosis. Diets contained approximately 500 mg/day cholesterol and 100 mg/day sitosterol. In the homozygote, plasma cholesterol and apolipoprotein B concentrations were slightly higher, but sitosterol levels were 22 and 58 times higher than in her heterozygous parents. Cholesterol absorption was at the high end of the normal range in both heterozygotes (59% and 84%) and in the homozygote (62%) (value in the control subject 48%). In contrast, cholesterol synthesis was severely depressed in the homozygote (28% and 26% as great as in the heterozygotes and the control, respectively). Sitosterol absorption in the homozygote (34%) was 2.3 and 2.0 times greater than in the heterozygotes and 6.8 times greater than in the control. The sitosterol turnover rate, calculated independently by mathematical analysis of specific-activity decay curves, amounted to 15 and 24 mg/day in the heterozygotes compared with 27 mg/day in the homozygote and 7.9 +/- 2.3 mg/day in five control subjects. However, the total body sitosterol pool was 15 and 10.3 times larger in the homozygote (4,080 mg) than in her heterozygous parents because of extremely slow removal. The average sitosterol elimination constant in the heterozygotes (KA = 0.11 day-1) was 10 times that in the homozygote (KA = 0.01 day-1) but 35% less than that in the controls (KA = 0.17 day-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1988

Competitive inhibition of bile acid synthesis by endogenous cholestanol and sitosterol in sitosterolemia with xanthomatosis. Effect on cholesterol 7 alpha-hydroxylase.

The 7 alpha-hydroxylation of two cholesterol analogues, sitosterol and cholestanol, and their effect on the 7 alpha-hydroxylation of cholesterol were measured in rat and human hepatic microsomes. In untreated rat liver microsomes, the 7 alpha-hydroxylation of cholesterol was higher than that of cholestanol (1.4-fold) and sitosterol (30-fold). After removal of endogenous sterols from the microsomes by acetone treatment, the 7 alpha-hydroxylation of cholesterol was similar to that of cholestanol and only fourfold higher than that of sitosterol. Cholestanol and sitosterol competitively inhibited cholesterol 7 alpha-hydroxylase in both rat and human liver microsomes, with cholestanol the more potent inhibitor. Patients with sitosterolemia with xanthomatosis, who have elevated microsomal cholestanol and sitosterol, showed reduced cholesterol 7 alpha-hydroxylase activity relative to the activity in control subjects (13.9 and 14.7 vs. 20.3 +/- 0.9 pmol/nmol P-450 per min, P less than 0.01). Enzyme activity in these patients was 40% higher when measured in microsomes from which competing sterols had been removed. Ileal bypass surgery in one sitosterolemic patient decreased plasma cholestanol and sitosterol concentrations and resulted in a 30% increase in hepatic microsomal cholesterol 7 alpha-hydroxylase activity. Cholesterol 7 alpha-hydroxylase appears to have a specific apolar binding site for the side chain of cholesterol and is affected by the presence of cholestanol and sitosterol in the microsomal substrate pool. Reduced bile acid synthesis in sitosterolemia with xanthomatosis may be related to the inhibition of cholesterol 7 alpha-hydroxylase activity by endogenous cholesterol analogues.

Adolescent↗
PubMed1992

Long-term treatment of severe familial hypercholesterolemia in children: effect of sitosterol and bezafibrate.

Seven prepubertal children (age range 5.3 to 10.8 years) with severe heterozygous familial hypercholesterolemia (serum cholesterol concentration 416 +/- 85 mg/dL and low-density lipoprotein [LDL] cholesterol concentration 360 +/- 90 mg/dL) were first treated by dietary intervention, second by sitosterol (3 x 2 g/d), and third by bezafibrate (2 x 200 mg/d). Each treatment period lasted 3 months. Subsequently, a treatment combining half the dose of sitosterol and bezafibrate was administered for the following 24 months. Diet alone reduced total and LDL cholesterol values by 4.5% (not significant) and 6.6% (P less than .05), respectively. Sitosterol lowered total and LDL cholesterol values by 17% (P less than .05) when compared with diet alone. Compared with sitosterol, bezafibrate produced a more pronounced effect on total and LDL cholesterol values (-18% and -28%, P less than .05), and high-density lipoprotein cholesterol concentration increased significantly from 48 mg/dL to 55 mg/dL. Combined treatment with half the dose each of sitosterol and bezafibrate was as effective as the higher dose of bezafibrate, and reduction averaged almost 40% and 50% for total and LDL cholesterol values; this lipid-lowering effect persisted for the next 24 months. Laboratory safety parameters and physical examination revealed no obvious side effects. This study indicates that the combination of sitosterol (3 x 1 g/d) plus bezafibrate (1 x 200 mg/d) is an alternate, acceptable, safe, and effective therapeutic approach for treatment of severe hypercholesterolemia in children with high-risk familial hypercholesterolemia.

Apolipoprotein A-I↗
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↗
PubMed1968

Quantitative aspects of the intestinal absorption and metabolism of cholesterol and beta-sitosterol in the rat.

The quantitative aspects of intestinal absorption and metabolism of cholesterol and -sitosterol have been studied in the rat after a single feeding of radioactive sterols. When increasing amounts of cholesterol were fed in a constant amount of triolein, the percentage absorbed decreased only gradually and the total amounts absorbed increased to a maximum. Solubility in the fat component fed is one limiting factor in the absorption of cholesterol. At the lowest dose fed, only about 50% of dietary cholesterol was absorbed even though increasing the amount fed led to a 10- to 15-fold increase in total absorption. Sitosterol, when fed in triolein, was absorbed in amounts only one-tenth of the corresponding dose of cholesterol. Intestinal transit studies indicate that the distinction between sitosterol and cholesterol, when fed together, took place during the process of uptake into the intestinal mucosa. Once taken up by the intestinal mucosal cells, cholesterol and sitosterol did not differ in their subsequent rate of transit out of the mucosal cell. Feeding sitosterol with cholesterol seems to have the same effect on cholesterol absorption as feeding the same additional dose of cholesterol, the difference being that sitosterol is taken up by the intestinal wall in amounts only one-tenth to one-fifth of that of cholesterol. The rapid and complete absorption of the triglyceride fat and the subsequent transit of the intestinal content to the large intestine are most probably important factors in the determination of the extent of absorption of nonglyceride fat. The mechanism behind the difference in extent of absorption of the closely related sterols is not explained.

Animals↗