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*
Unité des Maladies Métaboliques et Micronutriments, INRA de Clermont-Ferrand/Theix, 63122 St. Genès-Champanelle, France, and
Ross Products Division, Abbott Laboratories, Columbus, OH 43216
1To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • rats • cholesterol • bile acids • hydrocolloids
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Xanthan gum (XG) is a biosynthetic edible gum produced
by the bacterium Xanthomonas campestris; composed of
glucose, mannose and glucuronic acid. It has a coiled backbone and
tightly packed side groups while Konjac mannan (KM), obtained from the
tubers of Amorphophallus konjac, is a linear polymer of
mannose and glucose (Southgate 1976
). These two
compounds are also viscous fibers that are fermented in the large
intestine (Osilesi et al. 1985
, Vorster et al. 1985
).
The ability of soluble fibers to lower plasma cholesterol appears to be
due to different mechanisms. By increasing the viscosity of the digesta
and the thickness of the unstirred layer in the small intestine, fibers
can decrease cholesterol and bile acids absorption (Anderson et al. 1994
, Evans et al. 1992
, Gee et al. 1983
). Disturbance of the enterohepatic cycling of bile acids
is considered to be important in the cholesterol-lowering effect of
fibers. Increased fecal losses of bile acids likely induce bile acid
synthesis in the liver and hence accelerate cholesterol oxidation
(Stedronsky 1994
). This is generally accompanied by an
induction of hydroxymethylglutaryl CoA reductase (HMGR, a
rate-limiting enzyme of cholesterol synthesis), which is a response
to the channeling of hepatic cholesterol toward oxidation and/or
excretion (Arjmandi et al. 1992
, Levrat et al. 1996
, Pandak et al. 1990
). In parallel,
short-chain fatty acids (SCFA) resulting from microbial
fermentation of soluble fibers in the large bowel are absorbed in the
portal vein, and a major part is metabolized by the liver where
propionate especially can affect various metabolic processes
(Rémésy et al. 1995
). It has been proposed
that propionate could depress cholesterol synthesis. Although this
effect is relatively well documented in vitro, its relevance in vivo is
unclear (Demigné et al. 1995
, Stark and Madar 1993
, Stephen 1994
, Wolever et al. 1995
).
Rogel and Vohra (1983)
have reported that in chicks, 2%
of GG or KM in a semipurified diet containing 0.5% cholesterol reduced
plasma and hepatic cholesterol, compared to control chicks. Experiments
with hydrocolloids have frequently been carried out using a relatively
high percentage in the diet (seldom less than 5%), to achieve
substantial modifications of intestinal digestion and lipid variables.
However, humans cannot consume such quantities of viscous compounds,
and the amounts administered seldom exceed 10 g per day, which
corresponds to about 2.5% of the diet.
Thus, the purpose of this study was to determine if low levels of hydrocolloids in rats fed semi-purified diets would affect plasma lipid concentrations, and whether this depended on changes in the digestive balance of sterols and bile acids. All the diets were enriched with 0.2% cholesterol, and diets containing 1% GG, XG or KM were compared to a control fiber-free diet.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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56 male Wistar rats (IFFA-CREDO, L’Arbresle, France) that weighed
160 g were fed semi-purified diets that were distributed as a
moistened powder for 3 wk. Three diets containing fibers were compared
to a fiber-free diet. In the fiber-containing diets, 1% wheat
starch was replaced by 1% of either GG, XG or KM. Ingredients of the
four diets are listed in Table 1.
The rats were housed two per cage (wire-bottomed to limit coprophagy)
and maintained in controlled temperature rooms (22°C) with the dark
period from 2000 to 0800. Food consumption and growth rate were
measured twice weekly. For each cage, the feces were collected daily
during the last week. The rats were maintained and handled in
accordance with the recommendations of the Institutional Ethics
Committee.
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Forty rats were killed at 0900 at the beginning of the postabsorptive
period. They were anesthetized with sodium pentobarbital (40 mg/kg) and
maintained on a hot plate at 37°C. Blood was drawn into heparinized
syringes from the portal vein and abdominal aorta (
4 mL). Blood from
each rat was placed in a plastic tube containing heparin and
centrifuged at 10,000 x g for 2 min. After
centrifugation, plasma was removed and kept at 4°C for analysis.
After blood sampling, a portion of liver was freeze-clamped and stored at -20°C before extraction of lipids for determination of triglycerides (TG) and cholesterol. In parallel, 2 g liver was quickly homogenized in 4 mL of ice-cold buffer (mmol/L of Tris-HCl 50, mmol/L of sucrose 250, 50 mmol/L of EDTA, 2 mmol/L of dithiothreitol, and 1 µmol/L of leupeptin; pH 7.2) using a loose-fitting Teflon pestle. The homogenate was first centrifuged at 10,000 x g (15 min, 4°C); the resulting supernatant was then centrifuged at 100,000 x g (60 min, 4°C). The pellets were resuspended in 2 mL of the buffer, and the centrifugation procedure was repeated. The resulting pellets were homogenized in 1 mL of buffer A (100 mmol/L of sucrose, 50 mmol/L of KCl, 40 mmol/L of KH2PO4, 30 mmol/L of EDTA, and 1 mmol/L of dithiothreitol; pH 7.2). This microsomal preparation was stored at -80°C until measurement of HMGR activity. Protein content of the preparation was determined using the Pierce BCA Reagent kit (Interchim, Montluçon, France).
The cecum with content was removed and weighed. Each cecal content was transferred into two microfuge tubes; one was immediately frozen at -20°C and the cecal content pH was measured in the other. The cecal wall was flushed clean, blotted and weighted (cecal wall weight).
The other 16 rats were anesthetized with pentobarbital before the introduction of a PE 10 catheter into the bile duct. To measure the bile flow, they were maintained at 37°C, and bile samples were collected for 15 min in tared tubes. Samples were stored at -20°C until bile acid and cholesterol analyses were conducted.
Analytical procedures.
SCFA were measured by gas–liquid chromatography on plasma samples
after ethanolic extraction (Rémésy et Demigné 1974
) and on aliquots of supernatants of cecal contents (20,000
x g, 10 min at 4°C). Bile acid analysis was
performed on bile samples after a 30-fold dilution, on cecal contents
after sonication and extraction at 80°C for 1 h in 10 vol of
ethanolic KOH and on feces after two successive extractions at 80°C
(1 h in 10 vol of ethanolic KOH and 30 min in 3 vol of ethanol). Bile
acid concentration was measured on dilutions and on supernatants of
these extracts using an enzymatic method (3 
-hydroxysteroid
dehydrogenase; EC 1.1.1.50; Sigma, St. Louis, MO). Neutral steroids
were extracted three times with 1 mL hexane from a 100 µL aliquot of
the alkaline ethanolic extract. After addition of 5 -cholestane as
an internal standard, the solvent was evaporated under a stream of
N2 and the residue dissolved in hexane. Portions (0.5 µL)
of this extract were injected into a gas chromatograph (Daniducational,
Monza, Italy) equipped with a 12 m x 0.25 mm (inner diameter)
fused silica capillary column (BP10; SGE, Villeneuve-St.-Georges,
France) and a flame-ionization detector. Helium was used as a
carrier gas, and the sterols were separated using a gradient from 220
to 270°C (5°C/min). Sterols were calculated from the peak areas
relative to the peak area of the internal standard.
Plasma lipoproteins were separated by density gradient
ultracentrifugation (Sérougne et al. 1987
) using
pooled samples from 10 rats in each group (triplicate analysis). After
centrifugation in a TST 41.14 swinging-bucket rotor at 100,000
x g for 24 h at 18°C, the gradient was divided
into 24 x 500 µL fractions and kept at 4°C for lipid
analysis. Due to the low level of LDL and the relative overlapping of
HDL fractions in rat plasma, we decided to present data on the d<1.040
kg/L fraction [chiefly TG rich lipoprotein (TGRLP], (with a minor
contribution of LDL) and on the d>1.040 kg/L fraction (essentially
HDL).
TG and cholesterol were determined in plasma and lipoprotein fractions
by enzymatic procedures (PAP 150 and PAP1200 kits; BioMérieux
Charbonnières-les-Bains, France); cholesterol was also measured
in bile samples. Liver lipids were extracted with chloroform/methanol
(2:1; v/v) as described by Folch et al. (1957)
and
analyzed as described by Mazur et al. (1990)
. A
polyvalent control serum (Biotrol-33 plus, lot N° 577; Merck,
Chennevieres, France) was treated in parallel with the samples and
served as a control of the accuracy of results in TG and cholesterol
analysis. The activity of HMG CoA reductase (EC 1.1.1.34) was measured
on microsomal fractions as described by Wilce and Kroone (1992)
. Labeled mevalonolactone was separated from unreacted
HMG CoA by column chromatography, using AG1-X8 resin (200–400 mesh,
formate form; Biorad, Paris, France). Specific activity of the enzyme
was expressed in pmol [3-14C] HMG CoA transformed to
[14C] mevalonolactone/min/mg microsomal protein, after
correction for recovery of [3H] mevalonolactone from the
column.
Calculations.
The SCFA and bile acid cecal pools (µmol) were calculated as follows: cecal concentration (µmol/g) x cecal fresh content weight (g). The percentage of apparent cholesterol absorption was calculated as follows: (cholesterol daily intake - neutral sterols fecal daily excretion) x 100/cholesterol daily intake. Steroid balance was calculated by the difference between cholesterol intake and total steroids excretion (in µmol/d).
Statistical analysis.
Values are given as the means ± SEM. Data were tested by one-way ANOVA, and the Bonferroni/Dunn post-hoc test was used to determine significant differences among the means. Values were considered different at P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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There were no significant differences in the final rat body weight
after 21 d. They weighed about 300 g, corresponding to a
daily weight gain of 6.7 g/d (Table 2
).Food intakes did not differ among groups.
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Effects of diets on bile and cecal steroids.
The bile flow tended to be accelerated in rats fed the fiber diets
compared to controls (P = 0.08, Table 3
).The bile acid flux was significantly greater in the three groups fed
fiber diets (+35%, +58% and +49% with GG, XG and KM diets,
respectively) than in controls.
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Effects of diets on cholesterol intestinal absorption and steroid fecal excretion.
As shown in Table 4,
the fecal excretion of neutral sterols was markedly stimulated in rats
fed the hydrocolloids diets compared to rats fed the control diet,
especially in those fed the XG diet (+77%). KM was the least effective
(+35%), whereas GG had an intermediate effect (+57%). The major fecal
sterol was coprostanol; its excretion was 90% greater in rats fed XG
diet than in control rats. In rats fed GG or KM diets, its excretion
was only 70 or 57% greater (data not shown). Bile acid fecal excretion
was not significantly modified by diet and was markedly less than
neutral sterol excretion. Rats fed GG and XG diets had significantly
greater total steroid excretion (+35 and +46%, respectively) than
controls.
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). This
balance was strongly depressed in rats fed dietary hydrocolloids (-70,
-80 and -53% with GG, XG and KM, respectively, P < 0.05) but there was no significant difference among rats fed
hydrocolloids. The apparent cholesterol absorption (P
< 0.05) and apparent cholesterol digestibility were markedly
depressed in all groups fed hydrocolloids. Effects of diets on plasma and lipid concentrations and HMG CoA reductase activity.
Plasma cholesterol concentration was significantly lower in rats fed XG
(-23%) and GG (-14%) compared to rats fed the control diet; the KM
diet did not modify plasma cholesterol concentration (Table 5
).Only rats fed the XG diet had a lower plasma TG concentration than rats
fed the control diet (-22%); this value did not differ among rats fed
the three hydrocolloids diets.
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).The cholesterol-lowering effect of GG and XG was essentially found
in the d<1.040 kg/L fraction (TGRLP, plus some LDL), whereas
cholesterol in the d>1.040 kg/L fraction was not affected by any of
the diets. In the d<1.040 kg/L fraction, the TG concentration was
about 20% lower in rats fed the three fiber diets compared to those
fed the control diet. There was a significant correlation between
plasma cholesterol and total steroid excretion (r = -0.958, P = 0.042), but there was no significant
correlation for plasma TG.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). With the present low level in the diets, the three
fibers likely were completely fermented in the large intestine. The
molar ratio of cecal SCFA was not affected by the hydrocolloid diets,
yet GG can alter this ratio toward high-propionic acid
fermentations when present at a greater level in the diet
(Favier et al. 1995
). In the present study, differences
in the cecal propionate pool were small (from 54 µmol in controls to
about 75 µmol in rats fed fibers), and whether this could mediate
alterations in liver metabolism is uncertain since the propionate flux
to the liver was low.
It is noteworthy that a low percentage of hydrocolloid (1–2%) is
sufficient to lower plasma cholesterol in rats fed experimental diets
containing a moderate level of cholesterol (0.2%). The human Western
diet generally contains 3–4% total fiber (15–20 g/d for a 500 g/d of
dry matter intake). However, it has been suggested that the total
amount of dietary fermentable substrates could be higher than this
value, since a small proportion of dietary starch is
amylase-resistant (Englyst and Cumming 1986
,
Flourié et al. 1988
). Only a fraction of dietary
fiber has hydrocolloid characteristics and is liable to affect lipid
metabolism. Thus, providing 5 to 10 g of hydrocolloid daily as
purified fraction or consuming specific foods should double the intake
of gel-forming polysaccharides.
Rats are rather unresponsive to low levels of hydrocolloids when
fed cholesterol-free diets and, in this case, cholesterolemia is
not significantly altered. The mechanisms whereby soluble dietary
fibers may affect lipid metabolism have not yet been fully elucidated
(Schneeman 1998
), and several may be proposed to account
for the hydrocolloids’ effects including impaired cholesterol
absorption (Gee et al. 1983
, Simons et al. 1982
, Singh and Nityanand 1988
), increased
excretion of bile acids and sterols (Miettinen and Tarpila 1989
, Poksay and Schneeman 1983
, Vahouny et al. 1987
), altered cholesterol synthesis in the liver
(Arjmandi et al. 1992
) or accelerated uptake of
lipoprotein by the liver (Gatenby 1990
, Turner et al. 1990
). Hydrocolloids have the capacity to form a highly
viscous medium, which could alter lipid emulsification and lipolysis
(Pasquier et al. 1996
). The inhibitory effect of
hydrocolloids on cholesterol uptake might be merely due to reduced
diffusion or stirring of the solute in the fluid layer overlying
intestinal villi. Hydrocolloids may also interfere with cholesterol
transport by reducing the diffusion of the relatively large micelles,
or by binding cholesterol of the micelles (Vahouny et al. 1980
). Whatever the mechanism of action, the effect of
hydrocolloids on cholesterol apparent digestibility is important, since
this was decreased from 59% to 30% for XG and to 36% for GG and KM
diets. XG increased coprostanol and cholesterol excretions (+90% and
+58%, respectively), compared to control rats. Neutral sterols
accounted for a major part of steroid excretion, especially in rats fed
the hydrocolloids diets.
The biliary supply of endogenous cholesterol generally makes a
minor contribution to the total intestinal flux, but it may be
responsive to dietary cholesterol or hydrocolloids (Moundras et al. 1997
). In control rats and in rats fed the GG or KM diets,
the biliary secretion of cholesterol (extrapolated over 24 h)
corresponded to about 12% of the daily cholesterol excretion, but to
only 7% in rats fed the KM diet. Mucosal cell sloughing also
represents a source of endogenous cholesterol in the intestine, and
this source could be greater in rats fed hydrocolloid diets which cause
hypertrophy and accelerate turnover of the intestinal mucosa
(Ikegami et al. 1990
, Pell et al. 1992
).
It has been hypothesized that the cholesterol-lowering effect
of hydrocolloids could be due to an increase of the fecal excretion of
bile acids (Fernandez et al. 1995a
and
Fernandez et al.1995b
, Schneeman 1998
, Todd et al. 1990
). However, in the present
study, a low dose of hydrocolloid had a cholesterol-lowering effect
although fecal bile acid excretion was not significantly changed. After
extrapolating the biliary bile acid fluxes over 24 h, the fecal
loss of bile acids was relatively low representing 3.5% of the biliary
bile acid flux in rats fed the control diet and about 2% in the other
groups. Yet, hydrocolloids (even at the 1% level used)
enhanced the biliary flux of bile acids, due to small changes in both
bile flow and biliary bile acid concentration. Ebihara and Schneeman (1989)
reported that in rats fed a test meal
containing 5% GG or KM, bile acids are bound (or trapped) in the
intestine. Recently, it has been reported that GG diets may enlarge the
small intestine pool of bile acids (Favier et al. 1997
,
Moundras et al. 1997
). Thus, in rats fed hydrocolloids,
a greater proportion of bile acids would escape ileal reabsorption and
then reach the large bowel. In the cecum, passive bile acid
reabsorption may be facilitated by a greater surface area of exchange,
all the more since pH are not acidic enough to depress their
solubility. Enlarged bacterial mass may provide more binding
sites for bile acids (Gelissen and Eastwood 1995
) and could thus limit their passive absorption.
Nevertheless, it is conceivable that bile acid reabsorption in the
large intestine was at least as effective in rats fed the hydrocolloid
diets as in controls, as previously shown (Moundras et al. 1997
).
Hypocholesterolemia observed in rats fed GG and XG was caused by a
decrease of d<1.040 kg/L cholesterol fraction, whereas HDL cholesterol
was unaffected. This result is consistent with the lower apparent
cholesterol absorption we observed. In rats fed hydrocolloid diets,
high viscosity of the intestinal contents may delay lipid digestion,
promoting absorption in a more distal part of the small intestine
(Meyer and Doty 1988
), which may affect the size and apo
composition of TGRLP in rats (Mazur et al. 1990
,
Redard et al. 1992
). TG in the d<1.040 kg/L fraction
were significantly lower in rats fed 1% hydrocolloid diets, but it
must be kept in mind that blood was not sampled in food-deprived
rats but in rats at the beginning of the postabsorptive period. In
species with predominant LDL cholesterol, such as guinea pigs, GG
intake may accelerate VLDL and LDL apo B turnover and lower LDL apo B
flux (Fernandez et al. 1997
). In humans with moderately
raised plasma cholesterol concentration, supplementation of wheat bread
with GG lowered (-10%) plasma cholesterol, mainly as the result of a
reduction in the LDL-cholesterol fraction (Blake et al. 1997
). Liver is a major organ for cholesterol homeostasis in
rats because it can synthesize, oxidize or esterify cholesterol. In the
present study, GG and XG prevented hepatic cholesterol
accumulation while KG did not, in keeping with their potency to
increase fecal steroid excretion. When a diet contains cholesterol, HMG
CoA reductase should be severely down-regulated, all of the more
since exogenous cholesterol can fulfill the growth requirements
(estimated to about 30 µmol/d in the present conditions). In the
presence of hydrocolloids, the apparent steroid balance was markedly
reduced, but not sufficiently to elicit an induction of liver HMG CoA
reductase. In a previous experiment, 8% GG in a 0.4% cholesterol diet
decreased plasma and liver lipids and elicited a marked induction of
the hepatic HMG CoA reductase activity (Levrat et al. 1996
). It is also conceivable that acceleration of the
enterohepatic cycling of the bile acids, observed in rats fed the
hydrocolloid diets, prevents HMG CoA reductase induction.
In conclusion, agents such as GG or XG can reduce plasma cholesterol when present at a low percentage (1%) of the diet. Their cholesterol-lowering effect is probably tightly connected to their capacity to accelerate neutral steroid excretion, and these gums seem particularly effective in lowering the intestinal absorption of cholesterol. KM at 1% of the diet had only marginal effects on lipid metabolism, but this hydrocolloid might prove effective at a higher but still moderate dietary concentration.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Manuscript received February 17, 1999. Initial review completed March 26, 1999. Revision accepted October 7, 1999.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Anderson J. W., Jones A. E., Riddell-Mason S. Ten different dietary fibers have significantly different effects on serum and liver lipids of cholesterol-fed rats. J. Nutr. 1994;124:78-83
2. Arjmandi B. H., Ahn J., Nathani S., Reeves R. D. Soluble dietary fiber and cholesterol affect serum cholesterol concentration, hepatic portal venous short-chain fatty acid concentration and fecal excretion in rats. J. Nutr. 1992;122:246-253
3.
Blake D. E., Hamblet C. J., Frosyt P. G., Judd P. A., Ellis P. R. Wheat bread supplemented with depolymerised guar gum reduces the plasma cholesterol concentration in hypercholesterolemic human subjects. Am. J. Clin. Nutr. 1997;65:107-113
4. Demigné C., Morand C., Levrat M.-A., Besson C., Moundras C., Rémésy C. Effect of propionate on fatty acid and cholesterol synthesis and on acetate metabolism in isolated rat hepatocytes. Br. J. Nutr. 1995;74:209-219[Medline]
5. Ebihara K., Schneeman B. O. Interaction of bile acids, phospholipids, cholesterol and triglyceride with dietary fibers in the small intestine of rats. J. Nutr. 1989;119:1100-1106
6.
Englyst H. N., Cumming J. H. Digestion of the carbohydrate of banana in the human small intestine. Am. J. Clin. Nutr. 1986;44:42-50
7. Evans A. J., Hood R. L., Oakenfull D. G., Sidhu G. S. Relationship between structure and function of dietary fibre: a comparative study of the effects of three galactomannans on the cholesterol metabolism in the rat. Br. J. Nutr. 1992;68:217-229[Medline]
8. Favier M. L., Bost P. E., Guittard C., Demigné C., Rémésy C. The cholesterol-lowering effect of guar gum is not the result of a simple diversion of the bile acids toward fecal excretion. Lipids 1997;32:953-959[Medline]
9. Favier M.-L., Moundras C., Demigné C., Rémésy C. Fermentable carbohydrates exert a more potent cholesterol-lowering effect than cholestyramine. Biochim. Biophys. Acta 1995;1258:115-121[Medline]
10. Fernandez M. L. Distinct mechanisms of plasma LDL lowering by dietary fiber in the guinea pigs: specific effects of pectin, guar gum and psyllium. J. Lipid. Res. 1995a;36:2394-2404[Abstract]
11.
Fernandez M. L., Sun D. M., Tosca M., Mc Namara D. J. Guar gum effects on plasma low-density lipoprotein and hepatic cholesterol metabolism in guinea pigs fed low and high-cholesterol diets: a dose-response study. Am. J. Clin. Nutr. 1995b;61:127-134
12.
Fernandez M. L., Vergara-Jimenez M., Conde K., Behr T., Abdel-Fattah G. Regulation of apolipoprotein B-containing lipoproteins by dietary soluble fiber in guinea pigs. Am. J. Clin. Nutr. 1997;65:814-822
13. Flourié B., Leblond A., Florent C., Ratureau M., Bisalli A., Rambaud J. C. Starch malabsorption and breath gas excretion in the healthy human consuming low and high starch diets. Gastroenterology 1988;95:356-363[Medline]
14.
Folch J., Lees M., Sloane-Stanley G. H. A simple method for the isolation and the purification of total lipids from animal tissues. J. Biol. Chem. 1957;226:497-506
15. Gatenby S. J. Guar gum and hyperlipidaemia—a review of the literature. Leeds T. eds. Dietary Fibre Perspectives n°. 2 1990:100-115 John Libbey UK.
16. Gee J. M., Blackburn N. A., Johnson I. T. The influence of guar gum on intestinal cholesterol transport in the rat. Br. J. Nutr. 1983;50:215-224[Medline]
17. Gelissen I., Eastwood M. A. Taurocholic adsorption during non-starch polysaccharide fermentation: an in vitro study. Br. J. Nutr. 1995;74:221-228[Medline]
18. Ikegami S., Tsuchihashi F., Harada H., Tsuchihashi N., Nishide E., Innani S. Effect of viscous indigestible polysaccharides on pancreatic-biliary secretion and digestive organs in rats. J. Nutr. 1990;120:353-360
19. Levrat M. A., Moundras C., Younès H., Morand C., Demigné C., Rémésy C. Effectiveness of resistant starch, compared to guar gum, in depressing plasma cholesterol and enhancing fecal steroid excretion. Lipids 1996;31:1069-1075[Medline]
20. Mazur A., Rémésy C., Gueux E., Levrat M.-A., Demigné C. Effects of diets rich in fermentable carbohydrates on plasma lipoprotein levels and on lipoprotein catabolism in rats. J. Nutr. 1990;120:1037-1045
21.
Meyer J. H., Doty J. E. GI transit and absorption of solid food: multiple effects of guar. Am. J. Clin. Nutr. 1988;48:267-273
22. Miettinen T. A., Tarpila S. Serum lipid and cholesterol metabolism during guar gum, plantago ovata and high fibre treatments. Clin. Chim. Acta. 1989;183:253-262[Medline]
23.
Moundras C., Behr S. R., Rémésy C., Demigné C. Fecal losses of sterols and bile acids induced by feeding rats guar gum are due to greater pool size and liver bile acid secretion. J. Nutr. 1997;127:1068-1076
24.
Osilesi O., Trout D. L., Glover E. E., Harper S. M., Koh E. T., Behall K. M., O’Dorisio T. M., Tartt J. Use of xanthan gum in dietary management of diabetes mellitus. Am. J. Clin. Nutr. 1985;42:597-603
25. Pandak W. M., Heuman D. M., Hylemon P. B., Vlahcevic Z. R. Regulation of bile acid synthesis. IV. Interrelationship between cholesterol and bile acid biosynthesis pathway. J. Lip. Res. 1990;31:79-90[Abstract]
26. Pasquier B., Armand M., Guillon F., Castelain C., Borel P., Barry J.-L., Pieroni G., Lairon D. Viscous soluble dietary fibers alter emulsification and lipolysis of triacylglycerols in duodenal medium in vitro. Nutr. Biochem. 1996;7:293-302
27. Pell J. D., Gee J. M., Wortley G. M., Johnson I. T. Dietary corn oil and gum guar stimulate intestinal crypt cell proliferation in rats by independent but potentially synergistic mechanisms. J. Nutr. 1992;122:2447-2456
28. Poksay K. S., Schneeman B. O. Pancreatic and intestinal response to dietary guar gum in rats. J. Nutr. 1983;133:1544-1549
29. Redard C. L., Davis P. A., Middleton S. J., Schneeman B. O. Postprandial lipid response following a high fat meal in rats adapted to dietary fiber. J. Nutr. 1992;122:219-228
30. Rémésy C., Demigné C. Determination of volatile fatty acids in plasma after ethanolic extraction. Biochem. J. 1974;141:85-91[Medline]
31. Rémésy C., Demigné C., Morand C. Metabolism of short chain fatty acids in the liver. Cummings J. H. Rombeau J. L. Sakata T. eds. Physiological and Clinical Aspects of Short-Chain Fatty Acids 1995:171-190 Cambridge University Press UK.
32. Rogel A. M., Vohra P. Hypocholesterolemia and growth-depression in chicks fed guar gum and konjac mannan. J. Nutr. 1983;113(4):873-879
33. Schneeman B. O. Dietary fiber and gastrointestinal function. Nutr. Res. 1998;18:625-632
34. Sérougne C., Férézou J., Rukaj A. A new relationship between cholesterolemia and cholesterol synthesis determined in rats fed an excess of cystine. Biochim. Biophys. Acta 1987;921:522-530[Medline]
35. Simons L. A., Gayst S., Balasubramaniam S., Ruys J. Long term treatment of hypercholesterolemia with a new palatable formulation of guar gum. Atherosclerosis 1982;45:101-108[Medline]
36. Singh L., Nityanand S. Hypolipidemic effect of guar gum in rats and rabbits. Ind. J. Medic. Res. 1988;88:550-557
37. Southgate D.A.T. The chemistry of dietary fibre. Spiller G. A. Amer R. J. eds. Fibre in Human Nutrition 1976:31-42 Plenum New York.
38. Stark A. H., Madar Z. In vitro production of short-chain fatty acids by bacterial fermentation of dietary fiber compared with effects of these fibers on hepatic sterol synthesis in rats. J. Nutr. 1993;123:2166-2173
39. Stedronsky E. R. Interaction of bile acids and cholesterol with non-systemic agents having hypocholesterolemic properties. Biochim. Biophys. Acta 1994;1210:255-287[Medline]
40. Stephen A. Propionate-sources and effects on lipid metabolism. Binder A. Cummings J. Soergel K. eds. Short-Chain Fatty Acids 1994:260-271 Kluwer London.
41. Todd P. A., Benfield P., Goa K. Guar gum: a review of its pharmalogical properties, and use as a dietary adjunct in hypercholesterolemia. Drugs 1990;39:917-928[Medline]
42. Turner P. R., Tuomilehto J., Happonen P., La Ville A. E., Shaikh M. Metabolic studies of the hypolipidaemic effect of guar gum. Atherosclerosis 1990;81:145-150[Medline]
43. Vahouny G. V., Khalafi R., Satchithanandam S., Watkins D. W., Story J. A., Cassidy M. M., Kritchevsky D. Dietary fiber supplementation and fecal bile acids, neutral steroids and divalent cation in rats. J. Nutr. 1987;117:2009-2015
44.
Vahouny G. V., Roy T., Gallo L. L., Story J. A., Kritchevsky D., Cassidy M. Dietary fibers III. Effects of chronic intake on cholesterol absorption and metabolism in the rat. Am. J. Clin. Nutr. 1980;33:2182-2191
45. Vorster H. H., Kruger H. S., Frylinck S., Botha B. J., Lombaard W. A., De Jager J. Physiological effects of the dietary fibre component konjac-glucomannan in rats and baboons. J. Plant Foods 1985;6:263-274
46. Wilce P., Kroone P. A. Assay of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase. Converse C. A. Skinner E. R. eds. Lipoproteins Analysis 1992:203-214 Oxford University Press United Kingdom.
47.
Wolever T. M., Spadafora P. J., Cunnane S. C., Pencharz B. Propionate inhibits incorporation of colonic [1.213C] acetate into plasma lipids in humans. Am. J. Clin. Nutr. 1995;61:1241-1247
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