Fecal Bile Salt Research Articles

Hepatic Overexpression of Murine Abcb11 Increases Hepatobiliary Lipid Secretion and Reduces Hepatic Steatosis

Abcb11 encodes for the liver bile salt export pump, which is rate-limiting for hepatobiliary bile salt secretion. We employed transthyretin-Abcb11 and BAC-Abcb11 transgenes to develop mice overexpressing the bile salt export pump in the liver. The mice manifest increases in bile flow and biliary secretion of bile salts, phosphatidylcholine, and cholesterol. Hepatic gene expression of cholesterol 7alpha-hydroxylase and ileal expression of the apical sodium bile salt transporter are markedly reduced, whereas gene expression of targets of the nuclear bile salt receptor FXR (ileal lipid-binding protein, short heterodimer partner (SHP) is increased. Because these changes in gene expression are associated with an increased overall hydrophobicity of the bile salt pool and a 4-fold increase of the FXR ligand taurodeoxycholate, they reflect bile salt-mediated regulation of FXR and SHP target genes. Despite the increased biliary secretion of bile salts, fecal bile salt excretion is unchanged, suggestive of an enhanced enterohepatic cycling of bile salts. Abcb11 transgenic mice fed a lithogenic (high cholesterol/fat/cholic acid) diet display markedly reduced hepatic steatosis compared with wild-type controls. We conclude that mice overexpressing Abcb11 display an increase in biliary bile salt secretion and taurodeoxycholate content, which is associated with FXR/SHP-mediated changes in hepatic and ileal gene expression. Because these mice are resistant to hepatic lipid accumulation, regulation of Abcb11 may be important for the pathogenesis and treatment of steatohepatitis.

Hepatic overexpression of caveolins increases bile salt secretion in mice

Caveolins are cholesterol-binding proteins involved in the regulation of several intracellular processes, including cholesterol transport. Because hepatocytes express caveolin-1 and caveolin-2, these proteins might modulate hepatic lipid metabolism and biliary lipid secretion. Our aim was to investigate the potential physiologic role of caveolins in hepatic cholesterol and bile salt (BS) metabolism and transport using adenoviral gene transfer. C57BL/6 mice were infected with recombinant human caveolin-1 and caveolin-2 adenoviruses. Mice infected with adenovirus lacking the transgene were used as controls. Hepatic caveolin expression was evaluated by immunochemical methods. Reverse-transcription polymerase chain reaction (RT-PCR) and immunoblotting were used to assess messenger RNA (mRNA) levels and protein mass of BS transporters (sodium taurocholate cotransporting polypeptide [Ntcp] and bile salt export pump [Bsep]). Serum, liver, biliary, and fecal biochemical determinations and BS maximal secretory rate (SRm) were performed by standard methods. Ad.Cav-1- and Ad.Cav-2-infected mice exhibited a 10- and 7-fold increase in hepatic caveolin-1 and caveolin-2 protein expression, respectively. Caveolin-1-overexpressing mice had a significant increase in plasma high-density lipoprotein (HDL) cholesterol and hepatic free cholesterol content, whereas total plasma cholesterol and triglyceride levels remained unchanged. Hepatic caveolin-1 and/or caveolin-2 overexpression significantly increased bile flow and secretion of all biliary lipids. Caveolin-1-overexpressing mice showed a 2.5-fold increase in taurocholate (TC) SRm, indicating increased canalicular BS transport capacity. BS pool size and fecal BS excretion remained within the normal range in mice with Cav-1 overexpression. No changes were seen in the protein mass of BS transporters Ntcp and Bsep. In conclusion, our findings indicate that caveolins may play an important role in regulating hepatic BS and cholesterol metabolism. (H epatology 2003;38:1477-1488.)

Hepatic overexpression of caveolins increases bile salt secretion in mice.

Caveolins are cholesterol-binding proteins involved in the regulation of several intracellular processes, including cholesterol transport. Because hepatocytes express caveolin-1 and caveolin-2, these proteins might modulate hepatic lipid metabolism and biliary lipid secretion. Our aim was to investigate the potential physiologic role of caveolins in hepatic cholesterol and bile salt (BS) metabolism and transport using adenoviral gene transfer. C57BL/6 mice were infected with recombinant human caveolin-1 and caveolin-2 adenoviruses. Mice infected with adenovirus lacking the transgene were used as controls. Hepatic caveolin expression was evaluated by immunochemical methods. Reverse-transcription polymerase chain reaction (RT-PCR) and immunoblotting were used to assess messenger RNA (mRNA) levels and protein mass of BS transporters (sodium taurocholate cotransporting polypeptide [Ntcp] and bile salt export pump [Bsep]). Serum, liver, biliary, and fecal biochemical determinations and BS maximal secretory rate (SRm) were performed by standard methods. Ad.Cav-1- and Ad.Cav-2-infected mice exhibited a 10- and 7-fold increase in hepatic caveolin-1 and caveolin-2 protein expression, respectively. Caveolin-1-overexpressing mice had a significant increase in plasma high-density lipoprotein (HDL) cholesterol and hepatic free cholesterol content, whereas total plasma cholesterol and triglyceride levels remained unchanged. Hepatic caveolin-1 and/or caveolin-2 overexpression significantly increased bile flow and secretion of all biliary lipids. Caveolin-1-overexpressing mice showed a 2.5-fold increase in taurocholate (TC) SRm, indicating increased canalicular BS transport capacity. BS pool size and fecal BS excretion remained within the normal range in mice with Cav-1 overexpression. No changes were seen in the protein mass of BS transporters Ntcp and Bsep. In conclusion, our findings indicate that caveolins may play an important role in regulating hepatic BS and cholesterol metabolism.

Demonstration of a Direct Stimulatory Effect of Bile Salts on Rat Colonic Epithelial Cell Proliferation

Background: Despite the clear demonstration that an increase in faecal bile salt concentration can augment colonocyte proliferation, it is still controversial whether bile salts act on these cells as direct mitogens or by inducing a damage-related proliferative response. The goal of this study was to define the mechanism mediating the proliferative effect of bile salts on rat colonocytes. Methods: Faecal bile salt concentration was increased by feeding rats on diets enriched with either bile salts or fats. Colonic mucosa proliferating cell nuclear antigen (PCNA) expression, histology and apoptosis, and faecal water cytolytic activity were evaluated to assess proliferation and direct or indirect signs of mucosal damage. Results: Compared to standard diet, chenodeoxycholate-, deoxycholate- and fat-enriched diets produced a significant increase in both faecal water total bile salt concentration (46.0 versus 124.1, 145.9 and 498.5 μmol/L, respectively) and percentage of PCNA-positive nuclei (30.5, versus 37.7, 33.9 and 47.1, respectively) that appeared significantly correlated ( r s = 0.8; P < 0.001). Chenodeoxycholate and deoxycholate fed animals showed colonic mucosa histology and faecal water cytolytic activity similar to controls, with a significantly reduced apoptotic index. Rats fed on high fat diet, however, showed a mild inflammatory infiltrate associated with an increased apoptosis and faecal water cytolytic activity, all conditions not apparently determined by the increased faecal water total bile salt concentration. Conclusions: The results obtained in this study demonstrate that bile salts act as direct mitogens on colonic epithelial cells.

Effects on Cholesterol Balance and LDL Cholesterol in the Rat of a Soft-Ripened Cheese Containing Vegetable Oils

Objective: The purpose of this study was to examine effects of a modified soft-ripened cheese containing vegetable oils on cholesterol status, using the rat as the experimental model and the traditional soft-ripened cheese as the control.Methods: Adult male Wistar rats (≈370 g) were divided into two dietary groups (20 rats/group) and fed either the standard diet (STD, containing traditional cheeses made from whole milk) or the experimental diet (EXP, containing modified cheeses made from the combination of skim milk with the following fat mixture: milk fat/oleic acid-enriched sunflower oil/soybean oil mixture). Lipids of the diets came solely from cheeses (14 g/100 g diet); the EXP diet contained (3-fold) less saturated fat, (2-fold) less cholesterol, and (15-fold) more phytosterols than the STD diet.Results: Although serum triglyceride and total cholesterol concentrations were not affected by the type of diet, the EXP diet resulted in a significant reduction of LDL-cholesterol (31%, p<0.001) and a significant increase of HDL-cholesterol (11%, p<0.05), compared to the STD diet. Thus, a marked reduction (39%) of serum LDL/HDL cholesterol ratio was observed in the EXP group (p<0.001). In addition, the two quantitative balances (excreted/ingested) of cholesterol and total neutral sterols (for which phytosterols were excluded) were significantly higher by 183% and 174%, respectively for the EXP group, compared to the STD group (p<0.05). On another hand, rats fed the EXP diet excreted more cholesterol than they ingested dietary cholesterol (cholesterol balance ≷ 1), indicating that those animals eliminated some endogenous cholesterol in their feces, while the opposite was true for rats fed the STD diet (cholesterol balance < 1). Finally, fecal bile salt concentration was not significantly different between the two dietary groups.Conclusions: The partial substitution of milk fat by vegetable oils in soft-ripened cheese resulted in a decreased blood LDL/HDL cholesterol ratio and an increased fecal excretion of endogenous cholesterol and neutral sterols and, thus, markedly improved its nutritional qualities. Therefore, the consumption of the described modified cheese may meet the demand of subjects who wish to lower their risk for atherosclerosis and cardiovascular disease.

Effect of metformin on bile salt circulation and intestinal motility in Type 2 diabetes mellitus

Gastrointestinal symptoms can be a limiting factor in optimizing metformin therapy, particularly at the onset of treatment. The underlying cause remains unclear. We have investigated whether metformin changes oral-caecal transit and if it causes bile salt malabsorption using the lactulose breath test and orally administered 14C-glycocholate followed by breath 14CO2 measurement over 6 h and stool collection for 72 h, respectively. Twenty-four diet and/or sulphonylurea treated patients underwent 7 days of baseline investigations before entering a randomized double-blind crossover study of 21 days duration with either metformin (850 mg bd) or placebo. No difference was observed in the oral-caecal transit time but a change in fasting plasma glucose was observed of 2.6 mmol l−1 (95 % CI 1.3, 3.8). Significant increases in percentage 14CO2 breath elimination were observed during treatment with metformin (9.7 ± 6.3) compared with placebo (3.1 ± 1.9) p = 0.020. In addition, percentage faecal 14C bile salt excretion was increased with metformin (17.2 ± 9.9 vs 10.1 ± 6.9) p = 0.037. A significant association (p = 0.002) emerged for stool bile salt content and liquidity of the stool. We conclude that metformin may cause gastrointestinal disturbances by reducing ileal bile salt reabsorption leading to elevated colonic bile salt concentrations. © 1998 John Wiley & Sons, Ltd.

Pouchitis – What’s new in etiology and management

Pouchitis requires a clear clinicopathological definition. There are many conflicting data concerning etiology. It is linked to an initial diagnosis of ulcerative colitis by clinical association and occurrence of extra-alimentary manifestations, histologically and by macrophage types and inflammatory mediators. Evidence for a bacteriological cause comes from response to metronidazole, increased counts of intramucosal bacteria in pouchitis and the possible association of hypochlorhydria. Most studies have, however, shown no specific bacterial pathogen or luminal bacterial count differences in pouches with or without pouchitis. Abnormal fecal bile salt concentrations have been reported. Stasis and evacuation efficiency of the pouch are not associated with pouchitis in most studies. Reduced mucosal bloodflow may be associated perhaps leading to increased permeability to toxins causing activation of interleukin-1, platelet-activating factor (PAF) and tumour necrosis factor (TNF). PAF may be increased in pouchitis. Pouchitis may respond to allopurinol. Volatile short chain fatty acids (VSFA) may be reduced in ileal reservoirs compared with straight ileoanal segments and in pouchitis. The response of pouchitis to administered VSFA is, however, variable. Glutamine administration may help. There is evidence that intraepithelial T lymphocytes are reduced. Crypt cell turnover is higher in colitic than in polypotic pouches. Mucosal morphological changes of villous atrophy and inflammation occur early after relapsing polychondritis and may predict future susceptibility to pouchitis. Early mucosal biopsy appears to have prognostic value. Metronidazole and antibiotics (amoxicillin/potassium clavulanate, ciprofloxacin) may be effective although in a controlled trial of the former there was little advantage over placebo. The results of treatment using VSFA, glutamine, allopurinol sucralfate and anti-inflammatory agents, including aminosalicylic acid (5-ASA) and steroids, is reviewed. Assessment of efficacy is difficult because the definition of pouchitis is not standardized, there may be more than one clinical type and studies may not be controlled. Failure of medical treatment may require surgical defunctioning or removal of the pouch.

Fecal bile acids and neutral sterols in the cotton-top tamarin ( Saguinus oedipus)

1. 1. The cotton-top tamarin ( Saguinus oedipus), a small New World primate susceptible to spontaneous development of colon cancer, was studied for its fecal neutral sterol and bile salt composition. 2. 2. Standardization procedures to establish the effect of exposure of the stool to room temperature air for various time-periods showed no significant effects on the neutral sterol and bile salt composition of the samples. 3. 3. Microbial degradation of cholesterol and bile acids to secondary metabolites showed a progressive rise during the first year of life after which some degree of homeostasis was observed. 4. 4. The proportion of cholesterol that remained unmetabolized by colonic microflora was in excess of 50%, an amount that was significantly higher than in man and other higher primates. 5. 5. Ursodeoxycholic acid was identified as a significant (12%) component of fecal bile acids in this species. 6. 6. Secondary bile acids formed by the action of enteric microflora were also significantly lower than levels found in man and other animals.

Description and Simulation of a Multiple Mixing Tank Model To Predict the Effect of Bile Séquestrants on Bile Salt Excretion

A nonlinear, multicompartment mixing tank model based on human physiologic parameters from the literature and in vitro bile salt sequestrant binding parameters was integrated numerically to simulate bile salt excretion. The model focuses on the transit of bile salts and resin, bile salt binding, and bile salt reabsorption as a means of gaining insight into the functioning of bile sequestrants in the gastrointestinal tract and the effect of reabsorption of bile salts on the sequestering process. The series of compartments through the ileal region were tested over a range of parameter values, and the results were compared with bile salt output from ileostomy patient data to validate the model without resin. In simulations incorporating resin with a reversible binding scheme, fecal bile salt output was 2.37 (±0.6) x 10˜3 mol/day compared with 2.64 (±1.1) x 10˜3 mol/day for human data. Assuming irreversible bile salt binding resulted in predictions of fecal bile salt excretion greater than three times physiologic values. The results of these simulations support the hypothesis that the lack of efficacy of bile sequestrants is due to the displacement of bound bile salts from the sequestrant as a consequence of anion competition and bile salt reabsorption. Gastric emptying effects and the timing of resin doses have also been investigated with the model.

Growth of colorectal polyps

One hundred and sixteen patients were included, during 18 months, in a double-blind placebo-controlled intervention study, with calcium, vitamins A, C, E and selenium (in a cocktail) or placebo against growth of colonic polyps. Patients were randomized within three arms, according to diameter of the largest polyp, < 5 mm, 5-9 mm or > 9 mm. Polyps > 9 mm were resected, the others were left to be measured annually before resection after 3 years. The protocol (performed in all of the patients) included registration of demographic data, family and personal history, measurement of polyps, collection of blood specimens, stools and biopsy samples. Registration of nutritional status, diet history and 5-day prospective food consumption, was performed in 108 patients. The patient compliance was registered every third month by the hospital pharmacist, with concomitant delivery of new boxes of capsules. Additionally, stool collections were performed from all of the patients for the measurement of faecal calcium, bile salts and fat. Inclusion rate of 37, 41 and 38 patients in each of the three 6-month periods was uniform. The group with the largest polyps measuring 5-9 mm comprised 44% of the material. The sex ratio corresponded to that in overall referrals for colonoscopy. The age relationship of size and multiplicity of polyps and the distribution of polyps in the large bowel corresponded to previous experience in polyp-bearing individuals of the same age.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein B gene expression in rat intestine The effect of dietary fiber

The effect of the dietary fiber on apo B mRNA level was studied in the intestine of rats that were fed either fiber-free or high-fiber (30% sugar-beet fiber) low-fat diets for 3 weeks. The fiber diet studied does not affect jejunal apo B mRNA levels but decreases the level of ileal apo B mRNA. In the rat cecum, in both fiber-free and fiber groups, we failed to detect the apo B mRNA. The test fiber diet feeding markedly increased fecal bile salt and cholesterol excretions. We suggest that dietary fiber can modify apo B expression in the intestine. The increased fecal bile salt excretion might be involved in such a modification.

Effect of oral calcium on ileal bile salts

Bile acid excretion was measured in three ileostomates with and without oral supplements of calcium carbonate, 30–60 mmol/d. The ileal output of bile salts did not account for the doubling of fecal bile salts which is known to occur when these amounts of calcium carbonate are fed to intestinally intact subjects. Precipitation of bile salts in colonic contents appears to be the mechanism whereby oral Ca ++ increases fecal bile and excretion, and ameliorates the co-carcinogenic effects of bile salts on colonic mucosa.

Effects of intestinal microbial bile salt sulfatase activity on bile salt kinetics in gnotobiotic rats

Hepatic sulfation is thought to promote fecal excretion of lithocholate in humans by impairing the enterohepatic recirculation of the compound. Sulfatases produced by the gut flora may, at least in part, counteract this process. To investigate this interaction, female germfree rats, which are known to excrete considerable amounts of sulfated bile salts, were selectively associated with a bile salt desulfating flora. In these rats nearly all cecal, colonie, and fecal bile salt sulfate esters were hydrolyzed, resulting in a decrease of total fecal bile salt excretion of >25% compared with gnotobiotic rats without a bile salt desulfating flora. Desulfation of allochenodeoxycholate, the major sulfated bile salt in germfree rats, led to an enhanced recirculation and 12α-hydroxylation of the compound in the liver, resulting in an increased fecal output of allocholate. Microbial desulfation of intraperitoneally injected [24-14C]taurolithocholate-3-sulfate caused a fivefold decrease of the fecal plus urinary excretion rate of the isotope to approximately that found for unsulfated [24-14C]taurolithocholate. Coassociation of the gnotobiotic rats with a microflora that normalized the small intestinal transit time and cecal size led to a rise of total fecal bile salt excretion of >30% and a twofold accelerated excretion of both sulfated and unsulfated injected [24-14C]taurolithocholate. We conclude that in rats the gut flora rapidly desulfates intestinal bile salt sulfates, enhancing the enterohepatic recirculation and subsequent hydroxylation of the desulfated bile salts. In addition, these data illustrate the importance of having a well-defined microflora to normalize intestinal transit time and cecal size of gnotobiotic animals when performing kinetic studies of enterohepatic circulating compounds.

Bile Salt Malabsorption in Pancreatic Insufficiency Secondary to Alcoholic Pancreatitis

Twenty patients with exocrine pancreatic insufficiency secondary to alcohol abuse were studied for the presence of bile salt malabsorption. Fecal bile salts and fecal fat excretion were determined in 15 patients receiving pancreatic enzyme therapy, not receiving enzyme therapy, and on a regimen of pancreatic enzymes plus cimetidine. Serum bile salt levels were measured during fasting and postprandial conditions both during enzyme therapy and after it was stopped in 8 cases. In addition, 5 patients underwent [14C]cholylglycine breath testing during and after discontinuation of enzyme therapy. The fecal bile salt excretion varied between 610 and 3460 mg/day in the untreated patients. Treatment with pancreatic enzymes was associated with significant (p less than 0.05) reduction in fecal bile salt and fecal fat excretion. Cimetidine therapy in addition to enzyme therapy further reduced steatorrhea but failed to alter bile salt excretion significantly. Serum cholylglycine level showed significant (p less than 0.05) postprandial increase in patients receiving enzyme therapy, suggesting improved bile salt absorption. These data suggest a wide range of bile salt malabsorption in alcoholic patients with pancreatic insufficiency, which improves with pancreatic enzyme therapy.

Isolation of a rat intestinal Clostridium strain producing 5 alpha- and 5 beta-bile salt 3 alpha-sulfatase activity.

An unnamed sporeforming microorganism, termed Clostridium sp. strain S2, possessing bile salt sulfatase activity was isolated from rat intestinal microflora. The microorganism was a strictly anaerobic, nonmotile, gram-negative, asaccharolytic, sporeforming rod requiring CO2, vitamin K, and taurine; the guanine-plus-cytosine content of the DNA was 40.8 mol% (Tm), and the strain was tentatively classified as an atypical Clostridium species. Sulfatase activity was specific for 3 alpha-sulfate esters of 5 alpha- and 5 beta-bile salts, leaving the 3 beta-, 7 alpha-, and 12 alpha-sulfates unchanged. Strain S2 also deconjugated tauro- and glyco-conjugated bile salts and partially reduced into the corresponding 6 alpha-hydroxy bile salts. By these reactions, alpha-muricholate and beta-muricholate were more than 80% converted into hyocholate and omega-muricholate, respectively. In addition, strain S2 produced 12 alpha-hydroxysteroid dehydrogenase converting deoxycholate into 3 alpha-hydroxy-12-oxo-5 beta-cholanoate. When strain S2 was associated with gnotobiotic rats, the fecal bile salts were more than 90% desulfated and the fecal excretion of allochenodeoxycholate was five times lower than in control rats.

Influence of microbial bile salt desulfation upon the fecal excretion of bile salts in gnotobiotic rats

The fecal excretion of intraperitoneally injected 24- 14C-labeled taurocholate (TCA), taurolithocholate (TLCA) and the respective 3-sulfate esters (TCA-3-S; TLCA-3-S), were compared in germfree (GF) rats, conventional (CV) rats, and in gnotobiotic rats associated with Clostridium Cl-8 or this same strain Cl-8 plus the bile salt desulfating Clostridium S 1, respectively. TCA and TLCA were about two times more rapidly excreted by CV animals than by GF animals; the time required for 50% excretion of total label injected ( t 1 2 ) was 6.6 days vs 14.9 for TCA, and 4.4 vs 8.9 for TLCA. In GF and in CV animals, TCA-3-S and TLCA-3-S were excreted more rapidly than their nonsulfated analogues; the t 1 2 values of TCA-3-S and TCA were 2.7 days vs 14.9 in GF rats, and 3.1 vs 6.6 days in CV animals. The t 1 2 values of TLCA-3-S and TLCA were 2.7 days vs 8.9 in GF rats, and 1.5 vs 4.4 days in CV rats. In gnotobiotic rats associated with Clostridium strains S 1 + Cl-8, fecal bile salts were nearly 100% deconjugated and desulfated and the 50% excretion times of TCA-3-S and TLCA-3-S approximated to those of TCA and TLCA in GF animals. T 1 2 of TCA-3-S in gnotobiotic S 1, + Cl-8 animals was 12.2 days vs 14.9 for TCA in GF animals. In gnotobiotic S 1 + Cl-8 animals the t 1 2 of TLCA and TLCA-3-S was 12.5 and 11.0 days, respectively. These results illustrate clearly the important effect the intestinal microflora has upon the metabolic half-life of bile salts. Moreover, they demonstrate that desulfation of bile salts by the intestinal microflora takes place in intestinal segments from where a certain degree of reabsorption is still possible, and thus point to the fact that microbial desulfation is an important variable in the overall elimination of bile salts.

The Influence of Long‐term Cimetidine as an Adjuvant to Pancreatic Enzyme Therapy in Cystic Fibrosis

Seventeen patients on constant doses of pancreatic enzymes were randomised to receive either cimetidine or placebo for either of two successive six month periods. Nutritional state and maldigestion were assessed at the beginning and end of each period. Reductions in mean values of faecal fat, nitrogen, wet weight, and bile salts of approximately 30% were found on cimetidine therapy. Results showed considerable variation and only the fall in faecal fat was statistically significant. No benefit was demonstrated for height, weight, skinfold thickness, albumin, vitamin A, bone age or Crispin-Norman score.

Phototherapy-associated diarrhea. The role of bile salts.

The concentration of fecal bile salts was measured in 14 jaundiced neonates who received phototherapy (PT group) and their 14 nontreated matched controls (C). Before initiation of phototherapy, mean bile salt concentrations in stool specimens from the two groups were similar. At 12 hours of 'lights on', stool specimens from PT babies showed a significantly increased mean bile salt concentration, whereas in the C babies there was no change (3.65 +/- 0.39 vs 2.62 +/- 0.22 mmol/l; p less than 0.01). At 24 hours after 'lights off', stool specimens from the PT infants had a mean bile salt concentration like that before phototherapy, and not different from C. During phototherapy, nine PT babies had a bile salt concentration in their stools of 3.5 mmol/l and above; 6 of these babies had watery stools with a high sodium content. The high concentration of bile salts found in the colonic contents of neonates during phototherapy would appear to be a factor in the pathogenesis of phototherapy-associated diarrhea in the jaundiced neonate.

Effects of soy polysaccharide on gastrointestinal functions, nutrient balance, steroid excretions, glucose tolerance, serum lipids, and other parameters in humans

A diet-controlled study with a cross-over design was conducted to determine the effect of soy polysaccharide on gastrointestinal functions, nutrient balance, steroid excretion, blood lipid levels, postprandial serum glucose response, and other blood parameters in healthy male human subjects. A total of 14 college students was selected to participate in the study on a voluntary basis and each served as his own control. The study had two 17-day feeding periods. During the first feeding period, half of the subjects served as controls, the other as experimentais. During the second feeding period, treatments were crossed. When serving as controls, subjects consumed a low-fiber basal diet; when serving as experimentais, the same diet was supplemented with 25 g/day of soy polysaccharide. Blood samples taken at the beginning (days −1 and 1) and at the end (days 17 and 18) of each period revealed no changes in serum lipid levels or other blood parameters by soy polysaccharide supplementation. Nutrient balance and fecal transit studies revealed a significant increase in fecal wet weight and fecal water content, but no changes in total dry weight, fecal neutral steroid, bile salt, protein, and mineral contents. Glucose tolerance tests conducted during each period revealed that addition of soy polysaccharide to the glucose solution significantly reduced the reactive hypoglycemia at 180 min. Results of the present study suggest that in healthy male subjects, supplementation of soy polysaccharide can result in an increase in wet fecal content and possibly some improvement in glucose tolerance response.

Effect of guar feeding on the lipid profiles of hypercholesterolaemic rats and rabbits.

The significantly increased total cholesterol level of serum, liver and aorta of rats fed on hypercholesterolaemic diet was progressively lowered by the simultaneous administration of guar decoctions. When rabbits were first rendered hypercholesterolaemic and fed orally with guar decoction (equivalent to 40 g/kg), there was a significant lowering of both cholesterol and triglyceride levels of serum, liver and aorta which was comparable to the effect produced by clofibrate (50 mg/kg), associated with an increased excretion of faecal sterols and bile salts. The hypolipidaemic effect of guar may be attributed to its fibre content acting by decreasing cholesterol absorption and enhancing cholesterol break down.