Search PubMed⌕ Search

Biomedical subjects

S Wakabayashi

Publications and source records attributed to S Wakabayashi.

At least 55 records · Page 3Linked to original sources
PubMed1997

Change of mechanical activity to contraction from the relaxation induced by the intracellular Ca2+ antagonist KT-362; effects of alkylation of side chain, and substitution of 2,3,4,5-tetrahydro-1,5-benzothiazepine derivatives.

KT-362 (5-[3-[2-(3,4-Dimethoxyphenyl)ethyl]aminopropionyl]-2,3,4, 5-tetrahydro-1,5-benzothiazepine fumarate) is an intracellular Ca2+ antagonist. The compound obtained by introducing methyl groups onto the nitrogen (R2) of the side chain of KT-362 showed vasoconstrictive activity. Therefore we synthesized various derivatives, and examined their activities. Substitution at position R2 of the side chain resulted in potent contractile activity, and the optimal alkyl length was two or three carbons. The potency was further increased by the introduction of a chloro group at the R1 position of 2,3,4,5-tetrahydro-1,5-benzothiazepines. One of the synthesized compounds, 8-chloro-5-¿N-ethyl-N-[2-(3,4-dimethoxyphenyl)ethyl]aminopropionyl¿-2,3,4, 5-tetrahydro-1,5-benzothiazepine fumarate (9b), showed an EC50 value of 3.47 x 10(-8) M for contraction of rabbit iliac artery. The action of compound 9b was antagonized competitively by an H1-histamine receptor antagonist, diphenhydramine, and the pA2 value was 7.82. The maximum constriction was inhibited by a Ca2+ entry blocker, nicardipine, but not by an alpha 1-adrenoreceptor antagonist, prazosin. In a Ca(2+)-free medium, tonic constriction induced by 9b disappeared, and only a phasic constriction was observed. Though this phasic constriction was inhibited by diphenhydramine, it was not inhibited by prazosin or nicardipine.

Adrenergic alpha-Antagonists↗
PubMed1997

Three-dimensional imaging of cortical structure, function and glioma for tumor resection.

UNLABELLED: A three-dimensional brain imaging protocol with PET and MRI was used to visualize the cortical structure in relation to brain function and glioma infiltration to determine tumor resectability. METHODS: Sixteen patients with glioma had a PET scan with 11C-methionine to visualize tumor infiltration. The PET images were co-registered to the patients' own MRI reconstructed to the three-dimensional brain surface images to indicate the gyral structure and the extent of tumor infiltration. Thirteen patients, who bore tumors adjacent to the language or motor cortex, had H2 15O activation study to locate the eloquent cortex. The area of tumor infiltration was superimposed on the brain surface images together with the language and/or motor cortex. RESULTS: When a tumor was located within a single gyrus without influencing surface cortical gyrus pattern, the motor and language areas were identified morphologically by three-dimensional surface image alone. However, when the tumor caused swelling and deformation of cortical structure, functional mapping with H2(15)O activation technique was essential in locating them correctly. In such cases, the combined mapping of the facial motor area with oral movement and the language area with word repetition was the most useful method to identify the parasylvian structure in the dominant hemisphere. Total or near total resection of low-grade glioma in eight patients and the effective decompression of the active part of the malignant glioma in four patients was completed without causing functional neurological deterioration. CONCLUSION: The three-dimensional expression of cortical structure and function combined with PET glioma imaging with 11C-methionine is useful for radical resection of cerebral glioma.

Adult↗
PubMed1996

Phosphorylation-dependent regulation of cardiac Na+/Ca2+ exchanger via protein kinase C.

The cardiac Na+/Ca2+ exchanger (NCX1) plays a major role in the extrusion of Ca2+ from cardiomyocytes. We studied the role of protein phosphorylation in the regulation of cardiac NCX1 using CCL39 stably overexpressing the canine cardiac NCX1 and rat neonatal cardiomyocytes. In both cell types, the NCX1 protein immunoprecipitated with a chicken anti-NCX1 antibody exhibited a significant basal phosphorylation that was further enhanced by treatment with endothelin-1, acidic fibroblast growth factor, phorbol 12-myristate 13-acetate, or okadaic acid. In contrast, calphostin C, K252a, or EGTA inhibited the phosphorylation. The phosphorylation occurred on two major tryptic phosphopeptides (P1 and P2) exclusively on serine residues. Evidence is presented suggesting that P2 was derived from an N-terminal half (amino acids 240-475) of the central cytoplasmic domain of NCX1 and was phosphorylated directly by protein kinase C (PKC). The agents that increased NCX1 phosphorylation significantly enhanced both the forward and reverse modes of Na+/Ca2+ exchange. This exchange activation exhibited a very good correlation with the NCX1 phosphorylation. In NCX1-transfected cells, PKC down-regulation following prolonged exposure to phorbol 12-myristate 13-acetate abolished the acidic fibroblast growth factor-induced activation of exchange activity. On the other hand, cell ATP depletion reduced the exchange activity and abolished the effects of the above agents on exchange activity. These results indicate that the cardiac NCX1 is up-regulated by PKC-catalyzed phosphorylation. The cardiac NCX1 thus could play an important role in the previously reported negative inotropic actions of phorbol esters and other PKC-activating agents.

Adenosine Triphosphate↗
PubMed1996

Therapeutic effect of egualen sodium (KT1-32), a new antiulcer agent, on chronic gastritis induced by sodium taurocholate in rats.

We investigated the therapeutic effects of egualen sodium (KT1-32), a new antiulcer agent, on chronic erosive and atrophic gastritis induced by 5 months' administration of sodium taurocholate (TCA; 5 mM) in rats. The chronic gastritis was manifested by mucosal surface injuries (erosions), reduced mucosal thickness, reduction of the number of parietal cells, infiltration of inflammatory cells, and proliferation of collagenous fiber. Egualen sodium, (10-100 mg/kg, t.i.d.) administered orally to the rats for 2 weeks after the withdrawal of TCA, dose-dependently and significantly decreased the total length of erosions. The indicators of atrophic gastritis, i.e., reduced mucosal thickness and reduction in the number of parietal cells, were improved dose-dependently by the administration of this agent. Egualen sodium also reduced the inflammatory cell infiltration and the proliferation of collagenous fiber in the gastric mucosa in a dose-dependent manner. The reduced staining of neutral gastric mucus was improved by a high dose (100 mg/kg) of egualen sodium. The therapeutic effects of egualen sodium on experimental gastritis were superior to those of sofalcone and sodium guaiazulene 3-sulfonate. These results suggest that egualen sodium may be a promising agent for the treatment of erosive and atrophic gastritis.

Administration, Oral↗
PubMed1996

Azulene derivatives as TXA2/PGH2 receptor antagonists--II. Synthesis and biological activity of 6-mono- and 6-dihydroxylated-isopropylazulenes.

In order to examine the correlation between activity and hydrophilicity of the side chain of sodium 3-[4-(4-chlorobenzenesulfonylamino)butyl]-6-isopropylazulene -1-sulfonate (KT2-962), a non-prostanoid TXA2/PGH2 receptor antagonist, one or two hydroxyl groups were introduced into the isopropyl moiety. A series of 6-hydroxylated-isopropylazulenes were synthesized by regioselective oxidation of 6-isopropylazulenes and their in vitro and in vivo antagonistic activities were studied. Both the primary and tertiary alcohols, monohydroxylated derivatives, exhibited potent biological activities comparable to unmodified 6-isopropylazulenes both in vitro and in vivo. In contrast, the activities of 1,2- and 1,3-diols of 6-substituted derivatives, markedly decreased, but recovered by O-isopropylidenation of the dihydroxyl moiety. These findings indicate that the moderate hydrophobicity of substituent at the 6-position of the azulene ring might be required for the activity and the size of the substituent at this position, not so rigid for keeping potent biological activity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

[New intracellular calcium antagonists. I. Synthesis and pharmacological evaluation of 2,3,4,5-tetrahydro-1,5-benzothiazepine analogs].

A series of 2,3,4,5-tetrahydro-1,5-benzothiazepine and related compounds were prepared, and the intracellular Ca2+ inhibitory effects were examined using methoxamine- or caffeine-induced contraction of isolated rabbit arteries. Structure-activity relationship studies of these compounds are discussed and the results suggest that novel 5-[3-[2-(3,4-dimethoxyphenyl)ethyl]aminopropionyl]-2,3,4,5- tetrahydro-1,5-benzothiazepine fumarate (20d) showed the most potent inhibitory action on the intracellular Ca2+ release.

Animals↗
PubMed1995

Cytoplasmic domain of the ubiquitous Na+/H+ exchanger NHE1 can confer Ca2+ responsiveness to the apical isoform NHE3.

The Na+/H+ exchanger isoforms NHE1 and NHE3 are regulated differently by various stimuli. Calcium has been recognized as one of the major second messengers in such exchanger regulation. We previously proposed that Ca(2+)-induced activation of NHE1 occurs via displacement of its autoinhibitory domain from the H+ modifier site due to direct binding of Ca2+/calmodulin. To further validate this hypothesis, the functional role of the cytoplasmic domain was studied in both wild-type and chimeric exchangers, i.e. NHE1, NHE3, NHE1 with the cytoplasmic domain of NHE3 (N1N3), and NHE3 with the cytoplasmic domain of NHE1 (N3N1). After expression in exchanger-deficient fibroblasts (PS120), early response (< 80 s) to external stimuli was assessed as 5-(N-ethyl-N-isopropyl)amiloride-sensitive 22Na+ uptake. Among stimuli tested (ionomycin, alpha-thrombin, phorbol ester, hyperosmotic stress, and platelet-derived growth factor) that are all known to activate NHE1, only ionomycin and thrombin induced a significant intracellular Ca2+ mobilization and early activation of 22Na+ uptake, implying that Ca2+ is a main regulator of NHE1 in the early phase of the agonist response. However, all the stimuli did not activate NHE3 or N1N3. In contrast, a significant stimulation of 22Na+ uptake in response to ionomycin and thrombin was observed in N3N1, accompanied by an alkaline shift of pHi sensitivity (approximately 0.2 pH units). Deletion of the cytoplasmic calmodulin-binding domain within N3N1 resulted in a constitutive alkaline shift of pHi sensitivity and abolished the activation by ionomycin and thrombin. Together, these data reinforce our concept of Ca(2+)-induced activation of NHE1. Furthermore, they provide evidence for a functional interaction of the autoinhibitory domain of NHE1 with the H(+)-modifier site of a different isoform, NHE3.

Amiloride↗
PubMed1995

In vivo imaging of brain incorporation of fatty acids and of 2-deoxy-D-glucose demonstrates functional and structural neuroplastic effects of chronic unilateral visual deprivation in rats.

Regional cerebral 'incorporation coefficients' k* of each of 3 labeled long-chain fatty acids -[9,10-3H]palmitate ([3H]PA), [1-14C]arachidonate ([14C]AA) and [1-14C]docosahexaenoate ([14C]DHA)-were measured using quantitative autoradiography in 11 bilateral brain visual areas of 3.5-month-old awake, hooded, Long-Evans rats, and were compared with regional cerebral metabolic rates for glucose (rCMRglc). The rats, which had undergone unilateral orbital enucleation at 15 days of age, were studied either in the dark with eyelids of the intact eye sutured, or when stimulated in a light box with the intact eye open. rCMRglc did not differ between homologous contralateral and ipsilateral visual areas in the dark or during stimulation, but was elevated bilaterally by 25% or more in many visual areas during stimulation compared with dark. Contralateral compared with ipsilateral k* was lower for each fatty acid tracer in superficial gray of the superior colliculus (in dark and during stimulation) and dorsal nucleus of lateral geniculate body (during stimulation). In the dark, k* for [3H]PA was correlated significantly with rCMRglc for the 22 visual areas studied, whereas during stimulation k* for [14C]AA was correlated with rCMRglc. These results suggest that central neuroplastic changes following chronic unilateral enucleation are accompanied by reduced incorporation of [3H]PA, [14C]AA and [14C]DHA into contralateral brain ares that normally receive crossed retinofugal fibers, and by symmetry of rCMRglc in the dark but increased bilateral symmetrical responsiveness of rCMRglc to visual stimulation of the intact eye.

Animals↗
PubMed1995

Growth factor-induced phosphorylation and activation of aortic smooth muscle Na+/Ca2+ exchanger.

Although the Na+/Ca2+ exchanger is one of the major Ca2+ extrusion systems in excitable tissues, little is known about its regulation via protein phosphorylation. We now present evidence that the Na+/Ca2+ exchanger is phosphorylated in quiescent and growth factor-stimulated cultured aortic smooth muscle cells. The Na+/Ca2+ exchanger was isolated from 32P-labeled cells by immunoprecipitation with a specific polyclonal antibody. Phosphorylation of the exchanger was increased by up to 1.7-fold in response to platelet-derived growth factor-BB (PDGF-BB), alpha-thrombin, or phorbol 12-myristate 13-acetate (PMA). However, angiotensin II did not enhance the phosphorylation significantly. The extent of phosphorylation appeared to correlate with the growth factor-induced increase in cell 1,2-diacylglycerol. At least four phosphopeptides (P1 to P4) were detected by tryptic phosphopeptide map analysis of the phosphorylated exchanger, suggesting that phosphorylation occurred at multiple sites. PDGF-BB and PMA increased phosphorylation of the same phosphopeptides (in particular P1). Phosphorylated amino acids were exclusively serine residues in both quiescent and stimulated cells. We found that growth factors enhanced Na+/Ca2+ exchange activity and that there was a good correlation between the growth factor-induced stimulations of phosphorylation and exchange activity. PDGF-BB-induced activation of the exchanger was abolished by prior long treatment of cells with PMA. These results suggest that the Na+/Ca2+ exchanger is activated by protein kinase C-dependent phosphorylation in response to growth factors in vascular smooth muscle cells.

Animals↗
PubMed1995

Warfarin causes the degradation of protein C precursor in the endoplasmic reticulum.

Warfarin, an antagonist of vitamin K, is known to disrupt the microsomal vitamin K cycle, which results in a decrease in the plasma level of protein C, an anticoagulant factor, as well as some other vitamin K-dependent coagulation factors. Here, we examined the effect of warfarin on the secretion of recombinant protein C expressed in human kidney 293 or BHK cells. In transient expression, warfarin caused a 2-4-fold decrease in the quantity of protein C secreted, compared to findings with vitamin K-treated cells. Pulse-chase experiments using stable cells showed that, although recombinant protein C was secreted in the presence of vitamin K, the decrease in the total amount of radioactivity in the warfarin-treated cells suggested intracellular degradation. This degradation depended on the concentration of warfarin and was not inhibited by an endoplasmic reticulum (ER)-Golgi transport inhibitor (brefeldin A) or by lysosomotropic inhibitors (chloroquine and NH4Cl). Thus, protein C synthesized in the presence of warfarin is probably selectively degraded, and this degradation occurs in a pre-Golgi, nonlysosomal compartment. Among the protease inhibitors tested, N-alpha-acetyl-Leu-Leu-methioninal and N-alpha-acetyl-Leu-Leu-norleucinal blocked the degradation of protein C precursor synthesized in the presence of warfarin, and the precursor accumulated intracellularly, in a dose-dependent manner. Both inhibitors, however, did not disturb the secretion of protein C precursor in the vitamin K-treated cells. Thus, a cysteine protease(s) appeared to be responsible for the degradation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Subclinical renal oxalosis in wild-caught Japanese macaques (Macaca fuscata).

Various degrees of crystal deposition were found in the kidneys of 12 out of 59 Japanese macaques (Macaca fuscata) caught in the wild in Gifu, Japan. The needle- or rod-shaped crystals, which were radially arranged and occurred in the lumen and epithelium of the renal (mainly the proximal) tubules, were birefringent under polarized light. They stained with alizarin red S at a pH of 7.0 but not 4.2, and were identified as calcium oxalate. The morphological features of the renal lesions were similar to those previously reported in oxalate poisoning, and it was believed that the macaques ingested the oxalate in plants.

Animals↗
PubMed1995

Detachment of cultured cells from the substratum induced by the neutrophil-derived oxidant NH2Cl: synergistic role of phosphotyrosine and intracellular Ca2+ concentration.

The neutrophil-derived, membrane-permeating oxidant, NH2Cl, (but not the non-membrane-permeating chloramine, taurine-NHCl) induced detachment of fetal mouse cardiac myocytes and other cell types (fibroblasts, epithelial cells, and endothelial cells) from the culture dish, concomitant with cell shrinkage ("peeling off"). Stimulated human neutrophils also induced peeling off of cultured mouse cardiac myocytes when the latter were pretreated with inhibitors of .OH and elastase. Immunofluorescence microscopy revealed that the NH2Cl-induced peeling off of WI-38 fibroblasts is accompanied by disorganization of integrin alpha 5 beta 1, vinculin, stress fibers, and phosphotyrosine (p-Tyr)-containing proteins. Decrease in the content of the p-Tyr-containing proteins of the NH2Cl-treated cells was analyzed by immunoblotting techniques. Coating of fibronectin on the culture dish prevented both NH2Cl-induced peeling off and a decrease in p-Tyr content. Preincubation with a protein-tyrosine phosphatase inhibitor, sodium orthovanadate (Na3VO4), also prevented NH2Cl-induced peeling off, suggesting that dephosphorylation of p-Tyr is necessary for peeling off. NH2Cl-induced peeling off was accompanied by an increase in intracellular Ca2+ concentration ([Ca2+]i) in mouse cardiac myocytes and WI-38 fibroblasts. The absence of extracellular Ca2+ prevented both NH2Cl-induced peeling off and increased [Ca2+]i, both of which did occur on subsequent incubation of the cells in Ca2+-containing medium. These observations suggest that an increase in [Ca2+]i is also necessary for peeling off. Depletion of microsomal and cytosolic Ca2+ by incubation with the microsomal Ca2+-ATPase inhibitor 2',5'-di(tert-butyl)-1,4-benzohydroquinone (BHQ) plus EGTA prevented both NH2Cl-induced increases in [Ca2+]i and peeling off. Direct inhibition of microsomal Ca2+ pump activity by NH2Cl may participate in the NH2Cl-induced [Ca2+]i increment. A combination of p-Tyr dephosphorylation by genistein (an inhibitor of tyrosine kinase) and an increase in [Ca2+]i by BHQ could also induce peeling off. All these observations suggest a synergism between p-Tyr dephosphorylation and increased [Ca2+]i in NH2Cl-induced peeling off.

Animals↗
PubMed1995

Pharmacological properties of KT3-671, a novel nonpeptide angiotensin II receptor antagonist.

We examined pharmacological profiles of KT3-671, 2-propyl-8-oxo-1-[(2'-(1H-tetrazole-5-yl) biphenyl-4-yl)methyl]- 4,5,6,7-tetrahydro-cycloheptimidazole, a newly synthesized nonpeptide angiotensin II (AII) receptor antagonist in various in vitro and in vivo studies. KT3-671 displaced specific binding of [125I]Sar1 Ile8-AII to AT1 receptor with a Ki value of 0.71 +/- 0.14 x 10(-9) M in rat liver membranes, but had no affinity for AT2 receptor in bovine cerebellar membranes (Ki > 10(-5) M). In isolated rabbit aorta, KT3-671 produced a parallel rightward shift in the concentration-response curve for AII with a pA2 value of 10.04 +/- 0.12, but had no effect on KCl-, norepinephrine (NE)-, and serotonin (5-HT)-induced contractions. In conscious normotensive rats, KT3-671 (0.3-10 mg/kg, p.o.) inhibited the AII-induced pressor response dose dependently. In renal artery-ligated hypertensive rats, KT3-671 (0.1-3 mg/kg, p.o.) decreased arterial blood pressure (BP) dose dependently. The hypotensive action of 3 mg/kg KT3-671 was maintained for at least 24 h. These results suggest that KT3-671 is a potent AT1 subtype-selective and competitive nonpeptide AII receptor antagonist and has an orally active antihypertensive effect without agonistic activity.

Angiotensin II↗
PubMed1995

Responsiveness of mutants of NHE1 isoform of Na+/H+ antiport to osmotic stress.

Hypertonic activation of NHE1, the ubiquitous Na+/H+ exchanger, plays a central role in cell volume regulation, yet little is known about the underlying mechanism. We probed the osmotic responsiveness of full-length and truncated constructs of NHE1 transfected into cells lacking endogenous antiport activity. The hypertonic stimulation of NHE1 was preserved after heterologous transfection of the full-length NHE1 or of constructs truncated at positions 698 or 703. In contrast, mutants truncated at position 635 (delta 635) failed to respond to osmotic challenge. Transfectants (delta 635) behaved as if constitutively activated, having a permanently elevated cytosolic pH (pHi) under isotonic, unstimulated conditions. The delta 635 mutant displayed H+ binding with high affinity and low cooperativity. Constructs delta 582 or delta 566 had a reduced H+ sensitivity and were therefore inactive at resting pHi. Such cells were unresponsive to osmotic stress near physiological pHi but could be activated by shrinking after an acid load. Jointly, these results suggest that the H+ affinity and high cooperativity of the antiporter, earlier attributed to a single "modifier site," can be varied independently and are probably controlled by different regions of the molecule. The data indicate that volume or osmolarity-sensitive site(s) exist between the NH2-terminus and residue 566. This putative volume-sensitive site is therefore different from the site(s) postulated to mediate the stimulatory effects of calcium and growth factors.

Animals↗
PubMed1995

Basal cell tumor in a Japanese macaque (Macaca fuscata).

A rare case of basal cell tumor of the skin in a wild-caught female Japanese macaque (Macaca fuscata) was studied. Tumor growth, which was composed of cells resembling basal cells, was observed in the dermis and subcutis and showed a mixture of ribbon, solid, glandular, and cystic patterns. The tumor was separated from surrounding normal tissue by a compressed zone of fibrous connective tissue. The nuclei were round and hyperchromatic and possessed a single centrally located nucleolus. Mitotic figures were common. Immunohistochemically, a positive reaction for epithelial membrane antigen, keratin, and cytokeratin AE3 was evident. Electron microscopic examination revealed a small number of tonofilaments in the cytoplasm.

Animals↗
PubMed1995

Effects of indigestible dextrin on glucose tolerance in rats.

A recently developed indigestible dextrin (IDex) was studied for its effects on glucose tolerance in male Sprague-Dawley rats. IDex is a low viscosity, water-soluble dietary fibre obtained by heating and enzyme treatment of potato starch. It has an average molecular weight of 1600. An oral glucose tolerance test was conducted with 8-week-old rats to evaluate the effects of IDex on the increase in plasma glucose and insulin levels after a single administration of various sugars (1.5 g/kg body weight). The increase in both plasma glucose and insulin levels following sucrose, maltose and maltodextrin loading was significantly reduced by IDex (0.15 g/kg body weight). This effect was not noted following glucose, high fructose syrup and lactose loading. To evaluate the effects of continual IDex ingestion on glucose tolerance, 5-week-old rats were kept for 8 weeks on a stock diet, a high sucrose diet or an IDex-supplemented high sucrose diet. An oral glucose (1.5 g/kg body weight) tolerance test was conducted in week 8. Increases in both plasma glucose and insulin levels following glucose loading were higher in the rats given a high sucrose diet than in the rats fed a stock diet. However, when IDex was included in the high sucrose diet, the impairment of glucose tolerance was alleviated. Moreover, IDex feeding also significantly reduced accumulation of body fat, regardless of changes in body weight. These findings suggest that IDex not only improves glucose tolerance following sucrose, maltose and maltodextrin loading but also stops progressive decrease in glucose tolerance by preventing a high sucrose diet from causing obesity.

Animals↗
PubMed1995

Hypocholesterolemic effect of dietary fiber: relation to intestinal fermentation and bile acid excretion.

Rat cecal contents were static-cultured with three kinds of dietary fibers and examined for the production of short-chain fatty acids after 24h of cultivation. The total amount and molar ratio of acetate, propionate and butyrate (n = 8) were 7.20 +/- 0.62 mM and 38:19:43 with indigestible dextrin (ID), a low-viscosity, water-soluble dietary fiber, 10.88 +/- 0.46 mM and 49:5:46 with pectin (PE), a high-viscosity, water-soluble dietary fiber, and 1.83 +/- 0.19 mM and 64:11:25 with corn fiber (CF), a water-insoluble dietary fiber, respectively (the corresponding values obtained with glucose were 10.59 +/- 0.37 mM and 15:27:58). Next, rats were kept on a cholesterol- and bile acid-free high-sucrose diet. At the completion of the 8-week feeding period, the serum total-cholesterol levels were significantly lower, at 57.6 +/- 3.8 (n = 8), 63.2 +/- 4.67 (n = 7), and 77.8 +/- 3.7 mg/dl (n = 9), in the ID-, PE-, and CF-supplemented diet groups, respectively, than in the control group given no dietary fiber (92.7 +/- 3.8 mg/dl, n = 7). The cecal propionate production was significantly increased in both the ID and PE groups, while the fecal excretion of bile acids was increased in all three fiber groups compared to the control group. In addition, there was a significantly negative correlation between the serum total-cholesterol level and cecal propionate production in the ID group, between the serum cholesterol level and bile acid excretion in the CF group, and between the serum cholesterol level and cecal propionate production or bile acid excretion in the PE group. These results suggest that the degree of intestinal fermentation and bile acid excretion, which are considered to be associated with the hypocholesterolemic action of dietary fiber, varies with each kind of dietary fiber.

Acetates↗