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1.
The effects of feeding cholic acid, chenodeoxycholic acid and ursodeoxycholic acid on the activity of the hepatic steroid 12α-hydroxylase, gallbladder bile acid composition, fecal neutral sterol output, cholesterol synthesis and bile acid synthesis were determined in female hamsters. The 12α-hydroxylase activity was inhibited to 56% by cholic acid, to 62% by chenodeoxycholic acid, and to 78% by ursodeoxycholic acid compared with the control. Bile acid composition was altered by feeding of cholic acid and chenodeoxycholic acid to be rich in the given bile acids. Fecal neutral sterol output increased about twice by feeding chenodeoxycholic acid and ursodeoxycholic acid, whereas cholic acid had no significant effect. Body cholesterol synthesis increased to 217% by chenodeoxycholic acid and to 274% by ursodeoxycholic acid, whereas effect of cholic acid was not significant. Bile acid synthesis was suppressed to 48% of control only by chenodeoxycholic acid. A positive correlation between the 12α-hydroxylase activity and the bile acid synthesis was observed in the control, chenodeoxycholatefed and ursodeoxycholate-fed animals. In conclusion, ursodeoxycholic acid might have less inhibitory effect on the steroid 12α-hydroxylase and the bile acid synthesis than chenodeoxycholic acid. 相似文献
2.
Naoyuki Matoba Syoji Kuroki Bertram I. Cohen Erwin H. Mosbach Charles K. McSherry 《Lipids》1988,23(5):465-468
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. 相似文献
3.
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. 相似文献
4.
Shigeru Hashimoto Hirotsune Igimi Kiyohisa Uchida Takashi Satoh Yoshimi Benno Nozomu Takeuchi 《Lipids》1996,31(6):601-609
Wistar male rats were treated for six days with broad spectrum β-lactam antibiotics, latamoxef, and cefotaxime. On the seventh
day, the number of fecal anaerobic microbes decreased, total fecal bile acids decreased, and bile acid pools increased. Secondary
bile acids such as β-hyocholic, hyodeoxycholic, lithocholic, and deoxycholic acids decreased in the feces while the primary
bile acids, cholic, β-muricholic, and chenodeoxycholic acids, became predominant. Coprostanol, a microbial metabolite of cholesterol,
also disappeared from the feces during the treatment. The cecum enlarged to almost twice the size of that in control rats,
whereas the liver weight was not significantly changed. After treatment was stopped, the number of fecal microbes returned
to the initial counts within a week, but restoration of bile acid and cholesterol metabolism required at least three weeks. 相似文献
5.
Bertram I. Cohen Takahiro Mikami Nariman Ayyad Akira Ohshima R. Infante Erwin H. Mosbach 《Lipids》1995,30(9):855-861
The effects of β-muricholic acid and hyocholic acid on cholesterol cholelithiasis were examined in two animal models. The
following experiments were carried out: A) In a gallstone prevention study, prairie dogs were fed the lithogenic diet with
or without 0.1% β-muricholic or 0.1% hyocholic acid for eight weeks. B) In a second prevention study, hamsters were fed the
lithogenic diet with or without 0.1% β-muricholic acid or 0.1% hyocholic acid for six weeks. C) In a gallstone dissolution
study, hamsters were fed the lithogenic diet for six weeks to induce stones; stone dissolution was examined during administration
of a cholesterol-free purified diet with or without 0.1% β-muricholic acid or 0.1% hyocholic acid. In the prevention study
in prairie dogs (A), both bile acids failed to prevent stone formation, the cholesterol saturation index of bile was 0.89
in the lithogenic controls, remained unchanged with hyocholic acid and increased to 1.52 in the β-muricholic acid group. In
the prevention study in hamsters (B), β-muricholic acid completely inhibited the cholesterol cholelithiasis (0% stone incidence);
the cholesterol saturation index of bile was 1.78 (compared to lithogenic controls, 1.37). Hyocholic acid reduced stone incidence
to 16% with a cholesterol saturation index of 0.98. In the dissolution study in hamsters (C), preexisting cholesterol gallstones
were not dissolved by either hydrophilic bile acid after feeding these bile acids for an additional six weeks; at the end
of the experiment, the cholesterol saturation indices were below unity. These studies suggest that, in the hamster animal
model, hydrophilic bile acids may be useful for the prevention of gallstones but not dissolution of preestablished cholesterol
gallstones. 相似文献
6.
Yasuharu Imai Sumio Kawata Masami Inada Shio Miyoshi Yuzo Minami Yuji Matsuzawa Kiyohisa Uchida Seiichiro Tarui 《Lipids》1987,22(7):513-516
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. 相似文献
7.
Bertram I. Cohen Anil K. Singhal Richard J. Stenger Patricia May-Donath Judith Finver-Sadowsky Charles K. McSherry Erwin H. Mosbach 《Lipids》1984,19(7):515-521
The effects of 2 bile acid analogs, chenodeoxy-oxazoline [2-(3α,7α-dihydroxy-24-nor-5β-cholanyl)-4,4-dimethyl-2-oxazoline]
and ursodeoxy-oxazoline [2-(3α, 7β-dihydroxy-24-nor-5β-cholanyl)-4,4-dimethyl-2-oxazoline] were examined in the prairie dog
model of cholesterol cholelithiasis. Gallstones and biliary cholesterol crystals were induced in 5 out of 6 male prairie dogs
fed a semisynthetic diet containing 0.4% cholesterol for 8 weeks. Six animals maintained on a low cholesterol control diet
(0.08% cholesterol) exhibited neither gallstones nor biliary cholesterol crystals. The addition of 0.06% chenodeoxy-oxazoline
to the lithogenic diet did not prevent induced cholelithiasis or the appearance of cholesterol crystals in bile. In contrast,
0.06% dietary ursodeoxy-oxazoline prevented gallstones in 5 out of 6 prairie dogs (but cholesterol crystals were present in
the bile of 4 of these animals). Histologically, most of the livers from the prairie dogs fed the cholesterol-supplemented
semisynthetic diet showed bile duct proliferation, inflammatory infiltration and fibrosis along the portal tracts. These pathologic
changes were generally not ameliorated by adding chenodeoxy-oxazoline or chenodeoxy-oxazoline plus chenodeoxycholic acid to
the diet. Portal tract pathology was markedly reduced in most animals by adding ursodeoxy-oxazoline to the cholesterol-supplemented
diet. The pathologic changes overall could best be correlated with the presence of gallstones, but not with the incidence
of biliary cholesterol crystals. 相似文献
8.
Bertram I. Cohen Naoyuki Matoba Erwin H. Mosbach Richard J. Stenger Charles K. McSherry 《Lipids》1989,24(6):482-487
Dietary cholic acid (0.1%) and/or calcium (2.6% as calcium carbonate) were added to a semipurified diet containing cholesterol
and ethynyl estradiol to determine whether the incidence of pigment and/or cholesterol gallstones would be changed. Male golden
Syrian hamsters were fed the experimental diets for 96 days (Group 1, control; Group 3, cholic acid plus calcium) or only
an average of 60 days (Group 2, 0.1% cholic acid). Animals in Group 2 became ill (weight loss, low food intake, diarrhea)
possibly due to cholic acid (or deoxycholic acid) toxicity. Cholesterol gallstones and crystals were absent in all experimental
groups. The incidence of pigment gallstones was: control, Group 1, 12/16; 0.1% cholic acid, Group 2, 3/13; and 0.1% cholic
acid plus calcium, Group 3, 11/22. Cholic acid with or without calcium produced an elevation of both liver and plasma cholesterol:
Group 2, 80.1 mg/g and 501 mg/dl; Group 3, 103.7 mg/g and 475 mg/dl vs Group 1, 65 mg/g and 209 mg/dl, respectively. The lithogenic
indices of the bile were lower in Groups 2 and 3 compared to Group 1, controls, 0.45 and 0.58 vs 1.16, respectively. The extent
of the portal tract pathology could not be correlated with the presence or absence of pigment gallstones or with the levels
of lithocholic acid in the hamster bile. In summary, when semipurified diets were supplemented with ethynyl estradiol and
cholic acid, with and without calcium supplementation, no cholesterol gallstones formed and the incidence of pigment gallstones
was not altered. 相似文献
9.
In an established hamster model of cholesterol cholelithiasis, a semipurified lithogenic diet containing 4% butterfat and
0.3% cholesterol leads to the production of cholesterol gallstones in only 50–60% of animals after a 6-wk feeding period.
The purpose of this study was to investigate whether gallstone incidence could be increased while feeding a nutritionally
adequate diet of moderate cholesterol content. The semipurified lithogenic diet was modified as follows: (i) substitution
of 1.2% palmitic acid for 4% butterfat, and (ii) varying the amount of dietary cholesterol from 0.0 to 0.3% with either butterfat
or palmitic acid as the lipid component of the diet. Substitution of palmitic acid for butterfat produced a significantly
higher incidence of cholesterol gallstones (94%vs. 53%). Palmitic acid also raised the incidence of gallstones when added to the 0.1% and 0.2% cholesterol diets as compared
to butterfat: 0%vs. 44% and 50%vs. 81%, respectively. Gallstone incidence increased from 0% to nearly 100% when the cholesterol content of the palmitic acid
diets was raised from 0.0% to 0.3%, indicating a dose response effect with respect to dietary cholesterol. Hamsters fed cholesterol-free
diets did not form gallstones. Increased dietary cholesterol led to increased liver weight associated with a significant increase
in liver cholesterol concentration. However, the palmitic acid groups had significantly lower liver cholesterol values than
the corresponding butterfat groups. Serum and biliary cholesterol concentrations increased with increasing dietary cholesterol
intake, but there were no differences between the butterfat and palmitic acid groups. The cholesterol saturation index increased
from 0.56 to 1.32 in the butterfat groups and from 0.56 to 1.30 in the palmitic acid groups upon raising the dietary cholesterol
from 0.0 to 0.3%. Biliary total bile acid concentration did not vary significantly within all groups; however, the addition
of cholesterol produced an increase in the ratio of chenodeoxycholic acid to cholic acid. It is concluded that in Sasco hamsters
the saturated fatty acid, palmitic acid, when substituted for butterfat in a nutritionally adequate lithogenic diet, is capable
of increasing gallstone incidence to almost 100% during a 6-wk feeding period. 相似文献
10.
Bertram I. Cohen Erwin H. Mosbach Charles K. McSherry Beverly Rzigalinski Syoji Kuroki 《Lipids》1986,21(9):575-579
Gallstone formation and dissolution were studied in a prairie dog model of cholesterol (CH) cholelithiasis. Gallstones were
induced in 49 prairie dogs by feeding 1.2% CH in a nutritionally adequate semisynthetic diet for 6 wk (period 1). At 6 wk,
gallstones had developed in all animals examined. The diets were modified by reducing the amounts of CH to 0.4, 0.2, 0.1 and
0.0% (diets 1–4); hyodeoxycholic acid (HDA; 30 mg/kg/day) was added to these diets (diets 5–8). All animals were fed the modified
experimental diets for an additional 8 wk (period 2). At week 14, spontaneous gallstone dissolution had not occurred, even
in the groups given no added dietary CH during period 2 (group 4). Addition of HDA to the diet tended to reduce the incidence
of biliary CH crystals and the size and number of CH gallstones. Biliary CH remained elevated and the lithogenic indices in
all groups were found to be greater than 1.0 at the end of the experiment. Liver and plasma CH levels tended to be lower in
the groups fed HDA. In these groups, HDA and 6βHDA became the major biliary bile acids. This study demonstrates that HDA achieved
partial dissolution of gallstones in bile supersaturated with CH. 相似文献
11.
Bengt E. Gustafsson Bo Angelin Ingemar Björkhem Kurt Einarsson Jan-Åke Gustafsson 《Lipids》1981,16(4):228-233
The aim of this investigation was to study the influence of chenodeoxycholic acid administration on cholesterol and bile acid
synthesis in germ-free rats. Seven rats were fed a basal diet and 2 groups of 4 rats received the same diet supplemented with
0.4 and 1% chenodeoxycholic acid, respectively. After 6 weeks, feces were collected in one 3- and one 4-day pool for analysis
of cholesterol and bile acids. When the sampling period was finished, the rats were killed and the liver microsomal fractions
isolated. The activities of HMG CoA reductase and cholesterol 7α-hydroxylase were determined, the 7α-hydroxylase by a mass
fragmentographic method. The 2 dominating bile acids in the untreated rats were cholic acid and β-muricholic acid. During
treatment with chenodeoxycholic acid, 60–70% of this bile acid was converted into α- and β-muricholic acid, indicating a high
activity of the 6β-hydroxylase. The excretion of cholic acid was almost completely inhibited and the 7α-hydroxylase activity
was decreased ca 75% in the rats fed 1% chenodeoxycholic acid. The activity of the hepatic HMG CoA reductase was unchanged.
The fecal excretion of cholesterol increased 2–3 times. An accumulation of cholesterol was seen in the rats treated with 1%
chenodeoxycholic acid, which was probably a result of the decreased catabolism of cholesterol to bile acids. 相似文献
12.
Kiyohisa Uchida Haruto Takase Yasuharu Nomura Takashi Satoh Hirotsune Igimi Nozomu Takeuchi 《Lipids》1997,32(4):383-390
Serum cholesterol, triglyceride and phospholipid levels, liver cholesterol concentration, bile flow, biliary cholesterol,
phospholipid and bile acid secretion rates, fecal sterol and bile acid levels and their bile acid compositions were examined
in young-old parabiotic rats and compared with those in young and old control rats and young-young parabiotic rats. Bile acid
composition was expressed in terms of the cholic acid group/chenodeoxycholic acid group (CA/CDCA) ratio. Body weight (BW)
gain decreased after parabiosis especially in old rats, but the liver weight (g/100 g BW), diet-intake, feces dry weight,
liver cholesterol concentration and fecal sterol level were almost the same in all the groups. The biliary bile acid secretion
rate was higher and the fecal bile acid level was lower in old rats than those in young rats but both the levels became comparable
with those in young rats after parabiosis of old rats with young rats. Young rats, however, showed no changes in these levels
after parabiosis. The serum cholesterol level and the biliary and fecal CA/CDCA ratios in old rats were higher than those
in young rats but decreased after parabiosis with young rats, although they were still higher than those in young rats. The
serum cholesterol level in young rats increased after parabiosis with old rats, but not after parabiosis with young rats,
and the fecal bile acid level and the CA/CDCA ratio were not changed in either case. It is concluded from these findings that
the serum cholesterol level and the CA/CDCA ratio increased with age and that these increases were prevented after parabiosis
with young rats, while young rats, although their serum cholesterol level was increased, showed no increase in the CA/CDCA
ratio after parabiosis with old rats. 相似文献
13.
The effect of chenodeoxycholic acid, ursodeoxycholic acid and hyodeoxycholic acid on gallstone dissolution was studied in
the prairie dog. Cholesterol gallstones were found in all animals after feeding a semipurified diet plus 1.2% cholesterol
for six wk. Gallstone regression was examined by feeding a chow diet containing the bile acids (chenodeoxycholic acid, ursodeoxycholic
acid or hyodeoxycholic acid) alone (30 mg/kg/day) or in combination (chenodeoxycholic acid plus ursodeoxycholic acid) for
an additional six wk. Chenodeoxycholic acid was effective in dissolving established cholesterol gallstones (two out of 16
animals still had stones) and cholesterol crystals (six out of 16 animals had crystals); the hydrophilic bile acids, ursodeoxycholic
acid and hyodeoxycholic acid, were ineffective in the six-wk regression study. The lithogenic indices averaged 1.09 at the
end of the induction period: all biles became unsaturated with respect to cholesterol after the six-wk regression period (group
1, 0.82; group 2, 0.66; group 3, 0.81; group 4,0.84; group 5, 0.66). Cholesterol levels in liver, plasma and bile were elevated
after the six-wk induction phase (4.59 mg/g, 610 mg/dl and 0.36 mg/ml, respectively) but returned to near normal levels after
the six-wk regression period. Biliary bile acids contained increased levels of the dietary bile acid administered to each
group. This experiment shows that relatively hydrophobic bile acids may be more effective than hydrophilic bile acids for
gallstone dissolution during the period studied. 相似文献
14.
Glucose administered to fasted rats caused a marked stimulation in hepatic cholesterogenesis and cholesterol 7 alpha-hydroxylation, and an increase in biliary excretion of cholesterol and total bile acids. The excretion of cholic acid was not incluenced during the first few hr after glucose administration, but was significantly increased after 5 hr. Chenodeoxycholic acid showed a similar change, but the increase was only ca. one tenth of that of cholic acid. The excretion of deoxycholic acid was markedly increased by 1 hr, but gradually decreased thereafter. Pretreatment with neomycin abolished the increase in deoxycholic acid by fasting and glucose administration. Other bile acid components showed no significant change. It thus was presumed that cholesterol endogenously synthesized in the liver was metabolized mainly to cholic acid. In contrast, exogenous cholesterol was metabolized mainly to chenodeoxycholic acid. During the period of the acute enhancement of cholic acid formation from the endogenous cholesterol, biliary excretion of deoxycholic acid was increased. This probably occurred through the depression of 7 alpha-rehydroxylation of deoxycholic acid, or through the enhancement of microbial formation of deoxycholic acid in the lumen, and through the increase of intestinal absorption. 相似文献
15.
In the prairie dog model of cholesterol cholelithiasis, a high incidence of gallstones is achieved by feeding a semipurified
lithogenic diet containing 0.4% cholesterol for 2 mo. On occasion, we noted a decrease in the percentage of animals with gallstones
from 90–100% to 50–55%. To explain this phenomenon, we studied the effect of dietary history on gallstone formation. After
weaning, animals were fed either rodent chow or alfalfa plus corn (mo 0–3) followed by a cross-over experiment at mo 4–6.
Gallstone formation then was studied by feeding the lithogenic diet from mo 7 to 8. At sacrifice, the incidences of gallstones,
biliary lipids and tissue cholesterol levels were correlated with dietary history. The incidence of gallstones was 100% only
in animals fed the alfalfa-corn diet from weaning to 3 mo. In addition, the feeding of the alfalfa-corn diet at mo 4–6 increased
gallstone incidence from 65% to 86%. The lithogenic index of all groups was highest when the animals received only alfalfa-corn
prior to the lithogenic stimulus. The activity of hepatic HMG-CoA reductase was elevated in animals fed alfalfa-corn from
weaning to 8 mo, suggesting that this diet stimulates hepatic cholesterol synthesis, leading to increased biliary cholesterol
secretion. It is concluded that previous nutritional conditioning affects the incidence of gallstones. The prairie dog is
a useful model of cholesterol cholelithiasis, but the dietary history of the animals plays an important role in lithogenesis. 相似文献
16.
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. 相似文献
17.
Effects of bile acid feeding on hepatic deoxycholate 7α-hydroxylase activity in the hamster 总被引:1,自引:0,他引:1
In order to investigate the effects of bile acid feeding on hepatic microsomal deoxycholate 7α-hydroxylase activity, three
different bile acids were administered (0.2% w/w in chow) to hamsters for two weeks. Deoxycholate 7α-hydroxylase activity
was increased markedly by feeding of cholic acid (CA) and slightly by deoxycholic acid (DCA) Chenodeoxycholic acid (CDCA)
had little effect on the enzyme activity. Feeding each of the bile acids significantly inhibited the activity of cholesterol
7α-hydroxylase in the order CDCA≥ DCA>CA. There was no correlation between deoxycholate 7α-hydroxylase activity and cholesterol
7α-hydroxylase activity. It is concluded that the activity of deoxycholate 7α-hydroxylase is up-regulated by feeding DCA and
CA and that the mechanism seems to be different from that of cholesterol 7α-hydroxylase. The increased activity of hepatic
deoxycholate 7α-hydroxylase by CA and DCA should be beneficial in minimizing the toxic effects of DCA in the hamster. 相似文献
18.
Charles T. L. Huang M. M. Levine W. E. Woodward G. S. Gopalakrishna D. R. Nalin R. B. Hornick B. L. Nichols 《Lipids》1981,16(9):670-676
Fecal steroid compositions of 82 human subjects of various ages and diets and gastrointestinal status were examined by gas
liquid chromatography. Progressive increases in bacterial activities on both bile acids and neutral sterols were observed
with the advance of age in infants and children. The patterns in the 4-year-olds approached those observed in adults. Bacterial
activites on fecal steroids were found to be decreased in adult subjects with acute shigellosis and in those challenged by
castor oil. In contrast, no significant changes in fecal steroid profiles were observed in the subjects with traveller's diarrhea
assoicated with toxigenicEscherichia coli. The effects of diarrhea on fecal steroids of infants under 11/2 years were less consistent than those of adults. However, a close relationship was observed between the degree of 7α-dehydroxylation
of cholic acid (expressed as the ratio of deoxycholic to the sum of deoxycholic and cholic acids) and the percentage of cholesterol
in the feces (r= 0.921, p<0.001). The correlation between the production of lithocholic acid and the percentage cholesterol
was also good (r=−0.739, p<0.001). Analysis of neutral steroids may be a good index of intraluminal bile acid metabolism. 相似文献
19.
Effects of expansion of the hepatic free cholesterol pool on bile acid and cholesterol metabolism and homeostasis were examined
in rats fed cholesterol in high-fat diets or treated with oleyl-p-(n-decyl)-benzenesulfonate (ODS) or progesterone. Cholesterol feeding for 10–16 days, which increased free (33%) and esterified
(6-fold) cholesterol, had no effect on cholate synthesis, total bile acid synthesis, or cholate turnover, whereas these activities
were increased 60–80% by ODS and progesterone, which produced only small increases (19%) in free cholesterol. Cholesterol
feeding reduced β-hydroxy-β-methylglutaryl (HMG)-CoA reductase (72%) and cholesteryl ester hydrolase (48%) and increased acyl-CoA:cholesterol
acyltransferase (184%), whereas ODS and progesterone reversed these compensatory responses in cholesterol-fed rats. Cholesterol
7α-hydroxylase was changed no more than 22% by any treatment. A bolus of ODS elevated biliary cholesterol output 41% and shifted
biliary bile acid synthesis and composition toward 12-deoxy bile acids. These effects were not seen in ODS-fed or progesterone-treated
rats, in which cholesteryl ester stores were depleted. It is concluded that effects of free cholesterol on bile acid synthesis
and biliary cholesterol are probably mediated by specific precursor or regulatory pools which can be independently regulated
and which represent a relatively small fraction of hepatic free cholesterol. 相似文献
20.
This study examined the effect of castration and dietary hormonal supplementation on cholesterol cholelithiasis in male hamsters.
Animals fed a standard lithogenic diet developed cholesterol gallstones (17%) after 6 wk, while castrated hamsters did not
form any stones. Addition of a synthetic androgen, methyltestosterone, to the lithogenic diet induced cholelithiasis in castrated
animals (50%). The biles of normal and castrated-hormone supplemented hamsters had cholesterol saturation indices of 1.0 and
1.1, respectively, while the bile of the castrated animals remained unsaturated (0.6). The ratio of cholic acid/chenodeoxycholic
acid in bile increased after castration, but returned to normal levels following hormonal supplementation. Biliary cholesterol
carriers were separated by ultracentrifugation. Animals in the stone-forming groups (normal and castrated-hormone treated)
had a significant proportion of their biliary cholesterol in vesicles (44 and 46%, respectively); castrated hamsters had less
cholesterol in vesicle form (9%). The molar ratio of cholesterol/phospholipid in vesicles was reduced after castration (0.93
vs. 0.42) and increased by hormonal supplementation (1.89). In conclusion, when compared to normal male hamsters fed a standard
lithogenic diet, castration reduced the cholesterol saturation of bile, lowered the vesicular/micellar ratio in bile, and
inhibited cholesterol cholelithiasis. Dietary androgen supplementation increased the lithogenicity of bile, resulting in stone
formation in castrated animals. 相似文献