The cholesterol-lowering effect of guar gum is not the result of a simple diversion of bile acids toward fecal excretion

The effects of partially hydrolyzed, nonviscous, guar gum (PHGG) on cholesterol metabolism and digestive balance have been compared with those of native guar gum (GUAR) in rats adapted to 0.4% cholesterol diets. Both types of guar gum elicited acidic fermentations in the large intestine, but only GUAR effectively lowered plasma cholesterol (P<0.001), chiefly in the triglyceride-rich lipoprotein fraction. The biliary bile acid excretion was significantly enhanced in rats fed GUAR (P<0.05), as well as the intestinal and cecal bile acid pool (P<0.001). In rats fed GUAR and to a lesser extent in those fed PHGG, the fecal excretion of bile acids and neutral sterol was higher than in controls (P<0.01). The digestive balance (cholesterol intake-steroid excretion) was positive in control rats (+47 μmol/d), whereas it was negative in rats fed GUAR (−20 μmol/d), which could involve a higher rate of endogenous cholesterol synthesis. In rats fed PHGG, the steroid balance remained slightly positive. Liver 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity was very low (22 pmol/min/mg protein), owing to cholesterol supplementation, in control rats or in rats fed PHGG, whereas it was markedly higher (+463%) in rats fed GUAR. In conclusion, even if PHGG does alter some parameters of the enterohepatic cycle of cholesterol and bile acids, its effects are not sufficient to elicit a significant cholesterol-lowering effect. The intestinal (ileal or cecal) reabsorption of bile acids was not reduced, but rather increased, by GUAR; nevertheless the intestinal capacities of reabsorption were overwhelmed by the enlargement of the digestive pool of bile acids. In the present model, induction of HMG-CoA reductase probably takes place in the presence of elevated portal bile acid concentrations.     

Contrasting effects of water-soluble and water-insoluble dietary fibers on bile acid conjugation and taurine metabolism in the rat

The effect of the type of dietary fiber on the bile acid and taurine metabolism was examined in rats. Diets containing 10% of various water-soluble fibers (citrus pectin, konjak mannan, guar gum) as compared to a fiber-free diet increased biliary excretion of total bile acids. In contrast, water-insoluble dietary fibers (cellulose, corn bran, chitin; 10% in the diets) as well as cholestyramine (5% in the diet) considerably, decreased bile acid excretion. Water-soluble dietary fibermediated increases in bile acid excretion were totally attributable to increases in glycine-conjugates. Thus, these fibers greatly increased by the bile acid glycine-to-taurine ratio (G/T). Excretio of glycine conjugates decreased more than that of taurine conjugates in rats fed various water-insoluble dietary fibers. As a results, G/T in rats fed water-insoluble fibers was significantly lowered as compared to G/T in animals fed a fiber-free diet. Cholestyramine did not affect the G/T ratio of bile acids. Fecal bile acid excretion and the activities of hepatic cholesterol 7α-hydroxylase (EC 1.14.13.17) in rats fed various water-soluble dietary fibers approximately doubled as compared to the respective values for rats fed a fiber-free diet. Whereas cholestyramine greatly increased these parameters, water-insoluble fibers did not significantly affect them. Various water-soluble fibers decreased hepatic concentration and urinary excretion of taurine as well as the activity of hepatic cysteine dioxygenase (EC 1.13.11.20). In contrast, water-insoluble fibers considerably increased hepatic taurine concentrations and enzyme activities. The parameters for taurine metabolism were unaffected by cholestyramine. It was suggested that the types of dietary fiber affected hepatic taurine synthesis and thus modified bile acid glycine/taurine ratios.     

The cholesterol-lowering effect of guar gum in rats is not accompanied by an interruption of bile acid cycling

A viscous hydrocolloid (guar gum, GG; 2.5% of the diet) or a steroid sequestrant (cholestyramine; 0.5% of the diet) was included in semipurified diets containing 0.2% cholesterol to compare the cholesterol-lowering effects of each agent in rats. In the present model, GG significantly lowered plasma cholesterol (−25%), especially in the density <1.040 kg/L fraction, whereas cholestyramine was less potent. Bile acid fecal excretion significantly increased only in rats fed cholestyramine, similar to the cecal bile acid pool; the biliary bile acid secretion was accelerated by GG, but not their fecal excretion, whereas GG effectively enhanced neutral sterol excretion. As a result, the total steroid balance (+13 μmol/d in the control) was shifted toward negative values in rats fed the GG or cholestyramine diets (−27 or −50 μmol/d, respectively). Both agents induced liver 3-hydroxy-3-methylglutaryl-CoA reductase, but cholestyramine was more potent than GG in this respect. The present data suggest that, at a relative low dose in the diet, GG may be more effective than cholestyramine in lowering plasma cholesterol by impairing cholesterol absorption and by accelerating the small intestine/liver cycling of bile acids, which is interestingly, accompanied by reduction of bile acid concentration in the large intestine.     

Dietary fiber supplements: Effects on serum and liver lipids and on liver phospholipid composition in rats

Rats (6 per group) were fed semipurified diets containing either particulate fibers (alfalfa, 10%; cellulose, 10%; bran, 10%), a soluble ionic fiber (pectin 5%), soluble, nonionic fibers (guar gum, 5%; Metamucil, 10%), a mixed fiber preparation (Fibyrax, 10%, or an insoluble, ionic bile acid-binding resin (cholestyramine, 2%). The control group was fed the unsupplemented diet. The feeding period, during which diet and water were provided ad libitum, was 28 days. Compared with the control group, serum total cholesterol levels were increased by more than 10% in rats fed alfalfa and decreased by more than 10% in rats fed cellulose, guar gum, Fibyrax and cholestyramine. There were no significant differences in percentage of plasma HDL cholesterol. Serum triglycerides were elevated in the groups fed alfalfa, pectin, guar gum or Fibyrax and reduced in the group fed Metamucil. Plasma phospholipids were elevated in rats fed alfalfa or bran, unaffected in rats fed pectin or Metamucil and reduced in the other groups. Liver total cholesterol was elevated in all groups but those fed wheat bran and cholestyramine. The percentage of liver cholesterol present as ester was elevated in every group except that fed cholestyramine. Liver triglycerides were reduced in rats fed guar gum or Metamucil and elevated in those fed alfalfa. Liver phospho-lipids were lowered in the group fed cellulose. Liver phospholipids were fractionated by thin layer chromatography to give phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (Sph), lysophosphatidylcholine (LPC) and phosphatidylinositol plus phosphatidylserine (PI+PS). PC was elevated in all test groups (7–25%); PE levels ranged from 14% below to 0.3% above controls; Sph levels were sharply lower (20–53%) in all groups. LPC and PI+PS levels were close to the control value in all test groups. The results demonstrate that different dietary fibers can affect liver phospholipid composition. In view of the critical roles of phospholipids in many biological reactions, it will be interesting to survey the influence of dietary fiber on phospholipid spectra of other tissues. Deceased.     

Partially Hydrolyzed Guar Gums Reduce Dietary Fatty Acid and Sterol Absorption in Guinea Pigs Independent of Viscosity

This study investigated the effect of two partially hydrolyzed guar gums (PHGG) on fatty acid and sterol excretion. PHGG were obtained by chemical hydrolysis of guar gum (GG) with H₂O:EtOH (1:1) at 100 °C for 1 h (PHGG1) or 2 h (PHGG2). The viscosity of the PHGG in a 1 % (w/v) aqueous solution corresponded to that of a pseudoplastic fluid and was higher for PHGG1 than PHGG2. Guinea pigs (n = 8 per group) were fed high fat diets (17/100 g) that contained 12/100 g of cellulose, PHGG1, or PHGG2 for 4 weeks. Despite the differences in viscosity, the two PHGG exerted similar physiological effects. Compared to the control cellulose group, the body weight gain was lower in animals fed PHGG, although no effect on food consumption was observed. PHGG increased the excretion of fatty acids and neutral sterols, but not bile acids. Consumption of PHGG did not alter the fecal fatty acid profile, while intestinal bioconversion of sterols tended to increase in response to PHGG2. A reduction in the viscosity within the range tested did not correlate with losses in the hypocholesterolemic capacity of PHGG as both were effective in reducing plasma cholesterol. Thus, we conclude that the chemical hydrolysis of guar gum renders the gum suitable for inclusion in food products without significantly altering its beneficial health effects.     

Cholesterol synthesis and degradation in normal rats fed a cholesterol-free diet with excess cystine

Feeding a diet with excess cystine to rats resulted in hypercholesterolemia. To understand the mechanism of the hypercholesterolemia’ cholesterol synthesis and degradation’ bile acid content of bile’ and fecal steroids were determined. The in vivo incorporation of tritiated water into hepatic cholesterol’ and activity of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase in rats fed a high-cystine diet were significantly higher than those in rats fed a control diet. The activity of hepatic cholesterol 7α-hydroxylase was similar between two groups. Little effect of cystine supplementation was found on fecal sterol excretion although there were some changes in biliary excretion of cholic acid derivatives. These results indicate that hypercholesterolemia caused by feeding of a high-cystine diet may be due to the stimulation of hepatic cholesterol synthesis.     

Effect of 7-methylated bile acids and bile alcohols on cholesterol metabolism in hamsters

The effect of 7-methyl substituted bile acid and bile alcohol analogues on cholesterol metabolism was studied in the hamster. Animals were fed chow plus 0.1% cholesterol supplemented with 0.1% of one of the following steroids: chenodeoxycholic acid, 7-methyl-chenodeoxy-cholic acid, 7β-methyl-24-nor-5β-cholestane-3α,7α,25-triol, cholic acid, 7-methyl-cholic acid, or 7β-methyl-24-nor-5β-cholestane-3α,7α,12α,25-tetrol. Cholesterol absorption was determined from fecal analysis after feeding of radiolabeled cholesterol and β-sitosterol. Of the six compounds studied, chenodeoxycholic acid and 7-methyl-chenodeoxycholic acid decreased intestinal cholesterol absorption (17% and 31% decrease, respectively). Only 7-methyl-chenodeoxycholic acid decreased serum cholesterol concentration (29% decrease), but there were no analogous changes of liver and biliary cholesterol concentration and cholesterol saturation of bile. Total fecal neutral sterol excretion was increased in the groups fed chenodeoxycholic acid and 7-methyl-chenodeoxycholic acid. In addition, the production of coprostanol was increased in both groups. These data suggest that 7-methyl-chenodeoxycholic acid resembles chenodeoxycholic acid in its effect on cholesterol metabolism and may be a potential candidate for further studies of its gallstone-dissolving properties.     

Effectiveness of resistant starch,compared to guar gum,in depressing plasma cholesterol and enhancing fecal steroid excretion

Amylase-resistant starch (RS) represents a substrate that can be administered in substantial amounts in the diet, in contrast to gel-forming polysaccharides, such as guar gum (GG). The aim of this work was thus to compare the effects of GG and RS on cholesterol metabolism in rats adapted to 0.4% cholesterol diets, using dietary GG or RS levels (8 or 20%, respectively) that led to a similar development of fermentations, as assessed by the degree of enlargement of the cecum. The RS diet elicited a marked rise in the cecal pool of short-chain fatty acids, especially acetic and butyric acid, whereas the GG diet favored high-propionic acid fermentations. Both polysaccharides markedly altered the cholesterol excretion, from 50% of ingested cholesterol in controls, up to about 70% in rats adapted to the RS or GG diets. With these diets, the fecal excretion of bile acids was enhanced (67 and 144% with the RS and GG diets, respectively). RS and GG diets were effective in lowering plasma cholesterol (about −40%) and triglycerides (−36%). There was practically no effect of the diets on cholesterol in d>1.040 lipoproteins (high density lipoproteins), whereas RS (and to a larger extent, GG) were very effective to depress cholesterol in d<1.040 lipoproteins (especially in triglyceride-rich lipoproteins). Fermentable polysaccharides counteracted the accumulation of cholesterol in the liver, especially cholesterol esters. In parallel, liver acyl CoA:cholesterol acyltransferase was depressed in rats fed the RS or GG diets, whereas only the GG diet counteracted the downregulation of 3-hydroxy-3-methylglutaryl-CoA by cholesterol. These data suggest that RS may be practically as effective as a gel-forming gum, such as GG, on steroid excretion and on cholesterol metabolism.     

Sterol metabolism studies in rats: Effects of taurodeoxycholic acid feeding on sterol metabolism

Sterol metabolism studies using isotopic and chromatographic techniques were carried out in: (a) control rats fed stock chow +0.1% cholesterol (control group), and (b) rats fed stock chow +0.1% cholesterol and supplemented with 0.5% sodium taurodeoxycholate (taurodeoxycholate group). Feeding the bile acid enriched diet led to decreased acidic steroid synthesis, decreased cholesterol turnover, and cholesterol balance compared to nonsupplemented controls. There were no significant differences in fecal neutral sterol output, endogenous neutral sterol output, or cholesterol absorption between bile acid fed animals and controls. Tissue cholesterol levels (liver, plasma, and bile) in the two groups were also similar.     

Differential effects of ursodeoxycholic acid and ursocholic acid on the formation of biliary cholesterol crystals in mice

The preventive effect of 3α,7β,12α-trihydroxy-5β-cholanoic acid (ursocholic acid) and ursodeoxycholic acid on the formation of biliary cholesterol crystals was studied in mice. Cholesterol crystals developed with 80% incidence after feeding for five weeks a lithogenic diet containing 0.5% cholesterol and 0.25% sodium cholate. When 0.25% ursocholic acid or ursodeoxycholic acid was added to the lithogenic diet, the incidence as well as the grade (severity) of the gallstones were reduced. Plasma and liver cholesterol levels were decreased by ursodeoxycholic acid but not by ursocholic acid. Gallbladder cholesterol and phospholipid levels were decreased by both bile acids. The biliary bile acid level was decreased by ursocholic acid but not by ursodeoxycholic acid. After feeding ursocholic acid, its level in the bile was about 25% and the levels of cholic acid and β-muricholic acid decreased. Fecal sterol excretion was not changed by ursocholic acid, but was increased by ursodeoxycholic acid. After feeding ursocholic acid, fecal excretion of deoxycholic acid, cholic acid, and ursocholic acid increased. No differences were found between mice, with or without gallstones, in plasma and liver cholesterol levels, biliary phospholipid and bile acid levels, fecal sterol and bile acid levels, and biliary and fecal bile acid composition. The results suggest that the lower incidence of crystal formation after treatment with ursocholic acid is probably by a different mechanism than with ursodeoxycholic acid. In the mouse model, ursodeoxycholic acid exerts its effect at least partially, by decreasing cholesterol absorption. Ursocholic acid is well absorbed and excreted into bile and transformed into deoxycholic acid by the intestinal microflora in mice.     

Dietary fibers: V. Binding of bile salts,phospholipids and cholesterol from mixed micelles by bile acid sequestrants and dietary fibers

Mixed micelles were prepared containing combinations of either taurocholate or taurochenodeoxycholate, monoolein, oleic acid, dioleylphosphatidylcholine (lecithin) and cholesterol. These were incubated with commercial bile-acid-sequestering resins, cholestyramine and DEAE-Sephadex, or various dietary fibers and fiber components including wheat bran, cellulose, alfalfa, lignin and 2 viscosity grades of guar gum. Binding was determined as the difference between the radioactivity of each micellar component added and that recovered in the centrifugal supernatant after incubation. In general, the extent of bile salt sequestration was characteristic and reproducible for each bile salt, and was largely unaffected by the presence of one or more additional components of the micellar mixture, including the other bile salt. Cholestyramine bound 81–92% of the bile salts and 86–99% of the phospholipid and cholesterol present in micelles. DEAE-Sephadex sequestered only 49% of the taurocholate and 84% of the taurochenodeoxycholate, but completely removed all of the phospholipid and cholesterol from micelles containing either bile salt. Among the dietary fibers, guar gum of either viscosity bound between 20–38% of each micellar component, whereas lignin, alfalfa, wheat bran and cellulose were progressively less effective in sequestratin of individual components of mixed micelles. The extent of sequestration of micellar components by these resins and fibers is reasonably correlated with the effects of these same materials on lymphatic absorption of lipids and to their suggested hypocholesteremic properties.     

Pectin Penta-Oligogalacturonide Suppresses Intestinal Bile Acids Absorption and Downregulates the FXR-FGF15 Axis in High-Cholesterol Fed Mice

Haw pectin penta‐oligogalacturonide (HPPS), purified from the hydrolysates of haw pectin, has important role in decreasing hepatic cholesterol accumulation and promoting bile acids (BA) excretion in the feces of mice fed a high‐cholesterol diet (HCD). However, the mechanism is not clear. This study aims to investigate the effects of HPPS on BA reabsorption in ileum and biosynthesis in liver of mice. Results showed that HPPS increased fecal BA output by approximately 110%, but decreased ileal BA and the total BA pool size by approximately 47 and 36%, respectively, compared to HCD. Studies of molecular mechanism revealed that HPPS significantly decreased the mRNA and protein levels of farnesoid X receptor (FXR) in the small intestine of mice and inactivated the fibroblast growth factor 15 (FXR‐FGF15) axis, which increased the mRNA and protein levels of CYP7A1 by approximately 204 and 104%, respectively, compared to HCD. Interestingly, the mRNA and protein levels of apical sodium‐dependent bile acid transporter (ASBT) in the small intestine were approximately 128 and 73% higher in HPPS‐fed mice than those in HCD‐fed mice, respectively. However, no significant difference was detected for ASBT expression between HCD group and BA sequestrant cholestyramine group. These findings indicate that HPPS can suppress intestinal BA reabsorption and promoting hepatic BA biosynthesis. We speculated that HPPS could be ASBT competitive inhibitor rather than BA sequestrant in inhibiting BA reabsorption in ileum and improving cholesterol metabolism.     

The effects of polyoxyethylated cholesterol on fecal bile acids and nitrogen and on cholesterol balance in rats

Polyoxyethalated cholesterol (POEC) is a water soluble derivative of cholesterol which decreases cholesterol absorption in rats without affecting body weight, fatty acid excretion, or intestinal histology. In the present study rat feces were analyzed for cholic, deoxycholic, chenodeoxycholic, muricholic and lithocholic acid following 3 months of feeding a standard or a 2% enriched cholesterol diet with or without 1.5% POEC. In rats maintained on the cholesterol free diet, POEC increased total bile acids (mg/day) by 50% from 14±3 to 21±3 (mean ±SEM) but only the increase in chenodeoxycholic acid was significant (P<0.05). The corresponding POEC effect in the 2% cholesterol diet was 31% (70±8 to 93±3, P<0.01). Fecal nitrogen and serum cholesterol did not vary among groups. Comparing these data with neutral steroid excretion previously determined showed that POEC in the cholesterolfree diet increased the negative cholesterol balance more than three-fold (34±7vs 118±13 P<0.01). In rats fed 2% cholesterol, POEC caused a negative cholesterol balance of 222±8 compared to the control of 27±52 (P<0.01). The data indicate that POEC exerts complex effects in the intestinal tract which increase both bile acid and cholesterol excretion.     

Cholesterol binding capacity of fiber from tropical fruits and vegetables

The cholesterol binding capacity of 28 fiber samples from a variety of the more common tropical fruits and vegetables was determined. The binding capacity of cholestyramine, cellulose, lignin, guar gum and citrus pectin were also determined. Capacities were evaluated by an in vitro method that simulates the effect of the human digestive system on fiber using a series of enzymatic treatments before the binding was determined. Binding values varied from 3% for a soluble fraction of cassava to 84% for cholestyramine. Values for most fruit and vegetable fiber samples were less than or ca. equal to cellulose or lignin (20% and 16%, respectively). Apart from cholestyramine, sweet potato was the most effective binder (30%). Citrus pectin, at 8%, was a relatively poor binder. The capacity of guar gum (17%) was slightly less than cellulose. These data do not support the conclusion from in vivo studies that the hypocholesteremic effects observed for citrus pectin and guar gum are the result of the direct binding of cholesterol or bile acids in the large intestine. Southern Region, U.S. Department of Agriculture, Agricultural Research Service. Mention of a Trademark or proprietary product is for identification only and does not imply a guarantee or warranty of the product by the U.S. Department of Agriculture over other products that may also be suitable.     

Effect of cholestyramine on bile acid metabolism in conventional rats

Effects of cholestyramine on biliary secretion of cholesterol, phospholipids and bile acids and fecal excretion of sterols and bile acids were examined in Wistar male rats. Six rats were fed a basal diet, and the other six were fed a basal diet supplemented with 5% cholestyramine for eight days. Bile flow and biliary secretion of bile acids and phospholipids (per hour per rat) decreased with cholestyramine treatment, while biliary cholesterol secretion (per hour per rat) remained unchanged. In the biliary bile acid composition, a marked increase of chenodeoxycholic acid with a concomitant decrease of β-muricholic acid was observed in cholestyramine-treated rats. Fecal excretion of total sterols and bile acids increased about three-and four-fold, respectively, after cholestyramine treatment. The increase of fecal bile acids derived from cholic acid was more predominant than that derived from chenodeoxylcholic acid, resulting in an increase of the cholic acid group/chenodeoxycholic acid group ratio.     

Effect of chitosan feeding on intestinal bile acid metabolism in rats

The effect of chitosan feeding (for 21 days) on intestinal bile acids was studied in male rats. Serum cholesterol levels in rats fed a commercial diet low in cholesterol were decreased by chitosan supplementation. Chitosan inhibited the transformation of cholesterol to coprostanol without causing a qualitative change in fecal excretion of these neutral sterols. Increased fiber consumption did not increase fecal excretion of bile acids, but caused a marked change in fecal bile acid composition. Litcholic acid increased sigificantly, deoxycholic acid increased to a leasser extent, whereas hyodeoxycholic acid and the 6β-isomer and 5-epimeric 3α-hydroxy-6-keto-cholanoic acid(s) decreased. The pH in the cecum and colon became elevated by chitosan feeding which affected the conversion of primary bile acids to secondary bile acids in the large intestine. In the cecum, chitosan feeding increased the concentration of α-,β-, and ω-muricholic acids, and lithocholic acid. However, the levels of hyodeoxycholic acid and its 6β-isomer, of monohydroxy-monoketo-cholanoic acids, and of 3α, 6ξ, 7ξ-trihydroxy-cholanoic acid decreased. The data suggest that chitosan feeding affects the metabolism of intestinal bile acids in rats.     

An Egg-Enriched Diet Attenuates Plasma Lipids and Mediates Cholesterol Metabolism of High-Cholesterol Fed Rats

We investigated the influence of an egg-enriched diet on plasma, hepatic and fecal lipid levels and on gene expression levels of transporters, receptors and enzymes involved in cholesterol metabolism. Sprague–Dawley rats fed an egg-enriched diet had lower plasma triglycerides, total cholesterol, low density lipoprotein (LDL)-cholesterol, hepatic triglyceride, and cholesterol concentrations, and greater plasma high-density lipoprotein cholesterol concentration, fecal neutral sterol and bile acid concentrations than those fed a plain cholesterol diet. Chicken egg yolk had no effect on sterol 12α-hydroxylase and sterol 27α-hydroxylase; but upregulated mRNA levels of hepatic LDL-receptor, cholesterol 7α-hydroxylase (CYP7A1) and lecithin cholesterol acyltransferase, and downregulated hepatic hydroxymethylglutaryl-(HMG)-CoA reductase and acyl-CoA:cholesterol acyltransferase (ACAT) after 90 days. Modification of the lipoprotein profile by an egg-enriched diet was mediated by reducing de novo cholesterol synthesis and enhancing the excretion of fecal cholesterol, via upregulation of CYP7A1 and the LDL receptor, and downregulation of HMG-CoA reductase and ACAT.     

Effects of a single ingestion of sodium taurocholate on esterified cholesterol concentration in liver and cholesterol turnover in the rat

The overall response of the rat’s cholesterol metabolism to a single ingestion of taurocholate (80 mg) was studied with the isotopic equilibrium method. The bile acid production, measured by the daily¹⁴CO₂ output of rats in isotopic equilibrium of [26-¹⁴C]-cholesterol, initially decreased and then increased. Conversely, the hepatic concentration of esterified cholesterol first increased and then decreased. Moreover, the ingestion of taurocholate increasing the intestinal absorption coefficient of dietary cholesterol increased the abosprtion and decreased the fecal excretion and the intestinal biosynthesis of cholesterol. The balance of these last effects is an excess cholesterol inflow. The classical hypothesis of negative feedback regulation of bile acid production fails to explain the observed biphasic effect of taurocholate. This compound, when its origin is exogenous, appears to stimulate the storage of esterified cholesterol in the liver, at the expense of bile acid synthesis. This accumulation rate takes into account not only the decrease in cholesterol transformation into bile acids but also the excess inflow of cholesterol. As the exogenous taurocholate was eliminated from the body, cholesteryl ester hydrolysis occurred and provided a supplementary source of free cholesterol for bile acid synthesis.     

Effects of different levels of dietarytrans-octadecenoate on steroid metabolism in rats

Rats were fed semipurified diets containing olive oil or partially hydrogenated corn oil at the 5 or 20% level for ca. 30 days. These fat diets contained the same amount of octadecenoate but differed in the geometry with respect to each fat level. Contents oft-18∶1 were 26% and 41% of total fatty acids, respectively. The linoleic acid content was also made equivalent (3.8 energy %). After feeding on cholesterol-free diets, rats ontrans fat, compared to those oncis fat, showed: (a) no changes in serum cholesterol and apolipoprotein levels, (b) no effects on the bile flow and concentrations of biliary cholesterol or bile acids, (c) a trend toward increased fecal excretion of neutral and acidic steroids, (d) a lesser extent of transformation of cholesterol to coprostanol in the gut, and (e) no changes in the composition of biliary and fecal bile acids. Observations (c) and (d) were more marked with a hightrans fat regimen. These observations, except for serum apolipoproteins and fecal steroid excretion, were practically reproducible even when rats were fed cholesterol-enriched diets. A preliminary part of this study was presented at the 74th annual AOCS meeting, Chicago, 1983.     

Absorption, excretion, and distribution of plant sterols after proximal gut resection and autotransplantation of porcine ileum

Contribution of different gut segments to plant sterol absorption, adaptation of plant sterol absorption after partial small bowel resection, and effects of gut transplantation (necessitates extrinsic autonomic denervation and lymphatic disruption) on plant sterol biodynamics are unclear. We studied the consequences of massive proximal small bowel resection and autotransplantation of the remaining ileum on the adaptive absorption and biodynamics of plant sterols. Dietary, fecal, biliary, hepatic and plasma plant sterols, fecal elimination and absorption of cholesterol, small bowel morphology, and intestinal transit were determined before (n=5) and at 4, 8, and 14 wk after resection of the proximal 75% of the jejunoileum (n=15) and autotransplantation of the remaining ileum (n=15) or transection (n=5). Proximal gut resection significantly reduced cholesterol absorption efficiency; percentage absorption and biliary secretion of plant sterols; plasma, biliary and hepatic campesterol-to-cholesterol proportions; and sitosterol proportions in plasma and bile. Autotransplantation of the remaining ileum further significantly decreased cholesterol absorption efficiency; percentage absorption and biliary secretion of campesterol; campesterol proportions in plasma, bile and liver; and plasma proportions of sitosterol while increasing fecal excretion of neutral and acidic steroids. Plasma proportions of the two plant sterols, but absorption of just campesterol, were gradually improved with increasing cholesterol absorption and villus height after proximal gut resection; the same result was observed to a lesser degree after ileal autotransplantation. In addition, significant positive correlations were found between percentage cholesterol and campesterol absorption and the plasma plant sterol proportions in both proximal resection groups, between campesterol absorption and ileal villus height in the resection group, and between campesterol absorption and intestinal transit time in the autotransplantation group. In conclusion, plasma campesterol and sitosterol closely reflect absorption of cholesterol and plant sterols from intact and autotransplanted ileum during adaptation to proximal gut resection. A loss of proximal gut absorptive surface impairs cholesterol and campesterol absorption more than sitosterol absorption, the later being apparently less dependent on available jejunal villus surface area.