共查询到20条相似文献,搜索用时 31 毫秒
1.
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
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 influence of feeding cholesterol to rats during pregnancy and postpartum (from the 11th day of gestation to the third
day after delivery) on the serum and hepatic cholesterol levels and on the bile acid composition in the pool and in the liver
in relationship to the dams and their pups was examined. The hepatic content of cholesterol in both dam and offspring increased
during cholesterol feeding without any changes in serum cholesterol level. In the dams, mainly the esterified cholesterol
was increased; in the pups, mainly the free cholesterol was increased. Cholesterol feeding led to a pronounced increase in
the pool of β-muricholic acid and a relative decrease in the lithocholic acid concentration in pregnant rats. In fetal rats,
the chenodeoxycholic acid pool was increased by cholesterol intake. The lithocholic acid pool was larger in the postpartum
rats fed cholesterol than in the controls, while the concentration of α- and β-muricholic acids was decreased. The neonates
of cholesterol-fed dams had a larger pool of chenodeoxycholic acid but a smaller pool of β-muricholic acid. These results
suggest that the metabolism of cholesterol and of bile acids in dams and their offspring respond differently to cholesterol
intake. 相似文献
4.
The influence of phenobarbital on pool size and turnover of bile acids in rats have been investigated by administration of
[24-14C] cholic acid and tritium labeled chenodeoxycholic acid. Phenobarbital treated rats had a smaller cholic acid pool compared
to control rats (6.08±2.09 mg and 23.60±7.66 mg, respectively). The pool size of chenodeoxycholic acid, plus its metabolites
(α- and β-muricholic acids), was of the same magnitude in the two groups of animals. Also the daily production of cholic acid
was decreased in phenobarbital treated rats compared to control rats (2.12±0.46 mg and 7.24±1.66 mg, respectively). No significant
difference was observed between the synthesis of chenodeoxycholic acid in the two groups of animals. 相似文献
5.
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
6.
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
7.
Klyohisa Uchida Takashi Aklyoshi Hirotsune Igimi Haruto Takase Yasuharu Nomura Shouichi Ishihara 《Lipids》1991,26(7):526-530
The preventive effect of 3α,7β,12α-trihydroxy-5β-cholanoic acid (ursocholic acid) and ursodeoxycholic acid on the formation
of biliary cholesterol crystals was studied in mice. Cholesterol crystals developed with 80% incidence after feeding for five
weeks a lithogenic diet containing 0.5% cholesterol and 0.25% sodium cholate. When 0.25% ursocholic acid or ursodeoxycholic
acid was added to the lithogenic diet, the incidence as well as the grade (severity) of the gallstones were reduced. Plasma
and liver cholesterol levels were decreased by ursodeoxycholic acid but not by ursocholic acid. Gallbladder cholesterol and
phospholipid levels were decreased by both bile acids. The biliary bile acid level was decreased by ursocholic acid but not
by ursodeoxycholic acid. After feeding ursocholic acid, its level in the bile was about 25% and the levels of cholic acid
and β-muricholic acid decreased. Fecal sterol excretion was not changed by ursocholic acid, but was increased by ursodeoxycholic
acid. After feeding ursocholic acid, fecal excretion of deoxycholic acid, cholic acid, and ursocholic acid increased. No differences
were found between mice, with or without gallstones, in plasma and liver cholesterol levels, biliary phospholipid and bile
acid levels, fecal sterol and bile acid levels, and biliary and fecal bile acid composition. The results suggest that the
lower incidence of crystal formation after treatment with ursocholic acid is probably by a different mechanism than with ursodeoxycholic
acid. In the mouse model, ursodeoxycholic acid exerts its effect at least partially, by decreasing cholesterol absorption.
Ursocholic acid is well absorbed and excreted into bile and transformed into deoxycholic acid by the intestinal microflora
in mice. 相似文献
8.
Freshly isolated rat hepatocytes were used to examine the effects of dibutyryl cyclic AMP on the incorporation of14C-acetate and14C-cholesterol into bile acids. After an initial lag period, both precursors were incorporated into cholic and chenodeoxycholic
acids at a linear rate for the subsequent 60 min. An apparent stimulation of bile acid formation from14C-acetate by dibutyryl cyclic AMP was complicated by the concomitant inhibition of cholesterol synthesis. In experiments with14C-cholesterol, dibutyryl cyclic AMP (1 mM) increased the labeled cholic and chenodeoxycholic acids in the medium by 83 and
224%, respectively, but cellular levels of labeled bile acids were unchanged. As a result, the nucleotide stimulated the overall
incorporation of14C-cholesterol into cholic acid by 39% and into chenodeoxycholic acid by 123%. The mean ratio of labeled cholic to chenodeoxycholic
acid declined from 55∶45 in control cells to 41∶59 in cells incubated with dibutyryl cyclic AMP. The results demonstrate that
label incorporation can be used to study the regulation of bile acid synthesis in isolated hepatocytes. We propose that dibutyryl
cyclic AMP enhances bile acid production by phosphorylating, and thus stimulating the activity of, cholesterol 7α-hydroxylase,
the rate-limiting enzyme in bile acid synthesis. 相似文献
9.
Uchida K Satoh T Narushima S Itoh K Takase H Kuruma K Nakao H Yamaga N Yamada K 《Lipids》1999,34(3):269-273
The effects on bile acid and sterol transformation of clostridia (fusiform bacteria), the dominant intestinal bacteria in
rodents (ca. 1010 counts per g wet feces) were examined in Wistar rats. After inoculation of clostridia into germ-free rats and into rats previously
inoculated solely with Escherichia coli, most of the endogenous bile acids were deconjugated, and cholic acid and chenodeoxycholic acid were 7α-dehydroxylated to
deoxycholic acid and lithocholic acid, respectively. Tauro-β-muricholic acid, another major bile acid in rats, was deconjugated,
but only part of it (ca. 30%) was transformed into hyodeoxycholic acid. Cholesterol and sitosterol were also reduced to coprostanol and sitostanol,
respectively. Escherichia coli transformed neither bile acids nor sterols. These data suggest that clostridia play an imporant role in the formation of
secondary bile acids and coprostanol in rats. 相似文献
10.
Distribution and biliary and fecal excretion of bile acids were examined in Wistar strain male rats of about 300 g body weight.
The pool size of the rats on ordinary diet was 40 mg/rat, biliary secretion was 14 mg/hr, and fecal excretion was 10 mg/day.
Bile acids were mainly located in the small and large intestinal contents, 87% and 10%, respectively; but a portion was found
in the intestinal wall and the liver. Rats fed 2% cholesterol-supplemented diet for a week showed similar values for pool
size and biliary secretion with the rats on ordinary diet, but higher values for fecal excretion and distribution ratio in
the large intestinal contents. Cholic acid was a major component in the bile, small intestinal wall, small intestinal content
and liver, while the bile acid composition ratios were roughly similar to each other, although a relatively large amount of
α-muricholic acid was found in the intentinal wall and liver. Both the wall and content compositions of the large intestine
were similar to that of the feces, in which lithocholic, deoxycholic, α- and β-muricholic acids were the main components,
although the ratios of α- and β-muricholic acids in the large intestinal wall were larger than those in the intestinal contents
or feces. The high concentrations of these bile acids may indicate a difference of transport velocity across the cell membrane,
but the mechanism is not known. 相似文献
11.
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
12.
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
13.
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
14.
We investigated the influence of an egg-enriched diet on plasma, hepatic and fecal lipid levels and on gene expression levels
of transporters, receptors and enzymes involved in cholesterol metabolism. Sprague–Dawley rats fed an egg-enriched diet had
lower plasma triglycerides, total cholesterol, low density lipoprotein (LDL)-cholesterol, hepatic triglyceride, and cholesterol
concentrations, and greater plasma high-density lipoprotein cholesterol concentration, fecal neutral sterol and bile acid
concentrations than those fed a plain cholesterol diet. Chicken egg yolk had no effect on sterol 12α-hydroxylase and sterol
27α-hydroxylase; but upregulated mRNA levels of hepatic LDL-receptor, cholesterol 7α-hydroxylase (CYP7A1) and lecithin cholesterol
acyltransferase, and downregulated hepatic hydroxymethylglutaryl-(HMG)-CoA reductase and acyl-CoA:cholesterol acyltransferase
(ACAT) after 90 days. Modification of the lipoprotein profile by an egg-enriched diet was mediated by reducing de novo cholesterol
synthesis and enhancing the excretion of fecal cholesterol, via upregulation of CYP7A1 and the LDL receptor, and downregulation
of HMG-CoA reductase and ACAT. 相似文献
15.
Michel Riottot Philippe Olivier Anne Huet Jean-Jacques Caboche Michel Parquet Jamila Khallou Claude Lutton 《Lipids》1993,28(3):181-188
The effect of increasing amounts of a cyclic oligosaccharide, β-cyclodextrin (BCD), included in the diet on plasma cholesterol
and triglycerides, was investigated in two animal models, namely in male genetically hypercholesterolemic Rico rats and in
male Syrian hamsters. The distribution of bile acids in the gastrointestinal tract and in the feces of hamsters was also determined.
In the Rico rats and hamsters, plasma cholesterol and triglycerides decreased linearly with increasing doses of BCD. In these
two species, 20% BCD as compared to control diet lowered cholesterolemia (−35%) and triglyceridemia (−70%). In the hamster,
the BCD diet caused a marked decrease in cholesterol and triglycerides in chylomicrons and very low density lipoprotein, and
in high density lipoproteins cholesterol. Composition and amounts of bile acids were modified in the gastrointestinal tract
of hamsters receiving 10% BCD as compared to the control group. The total bile acid content of the gallbladder of treated
hamsters was fourfold higher than in the control group, and the bile contained a large amount of hydrophilic bile acids. This
trend was also observed in the small intestine, in which percentages and total quantities of cholic plus deoxycholic acids
(cholic pathway) were higher than those of chenodeoxycholic plus ursodeoxycholic plus lithocholic acids (chenodeoxycholic
pathway). The bile acid contents of the cecum and colon of treated hamsters were 2.7-fold higher than those of control animals,
but the bile acid composition was similar in the two groups of hamsters. Fecal excretion of bile acids was 3.3-fold higher
in the treated group than in the control group, and the percentage of lithocholic acid was markedly increased and close to
that observed in the colon. The turnover of the chenodeoxycholic pool was twice as fast in treated hamsters as in control
hamsters, whereas that of cholic acid was not significantly modified. These results suggest that BCD does not alter the microbial
degradation of bile acids, but rather stimulates their synthesis and increases their pool size. BCD prevents the intestinal
absorption of lithocholic acid and washes this cytotoxic bile acid from the colon. The hypocholesterolemic effect of BCD appears
to be due to stimulation of bile acid synthesis. 相似文献
16.
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
17.
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
18.
Jan Gustafsson 《Lipids》1980,15(2):113-121
Conversion of 3α,7α,12α-trihydroxy-5β-cholestanoic acid into 3α,7α,12α24-tetrahydroxy-5β-cholestanoic and cholic acids was
catalyzed either by the mitochondrial fraction fortified with coenzyme A, ATP, MgCl2 and NAD or by the combination of microsomal fraction and 100,000 x g supernatant fluid fortified with coenzyme A, ATP and
NAD. 24-Hydroxylation and formation of cholic acid occurred at similar rates with the 25R- and the 25S-forms of 3α,7α,12α-trihydroxy-5β-cholestanoic
acid. The 25R- and 25S-forms of 3α,7α,12α-trihydroxy-and 3α,7α,12α,24-tetrahydroxy-5β-cholestanoic acids were administered
to bile fistula rats. Labeled cholic acid was isolated from the bile. The initial specific radioactivity of cholic acid was
higher and the disappearance of radioactivity more rapid after administration of 3α,7α,12α-trihydroxy-5β-cholestanoic acid
than of 3α,7α,12α,24-tetrahydroxy-5β-cholestanoic acid. The findings are discussed in relation to the assumed pathway for
side chain cleavage in cholic acid biosynthesis. 相似文献
19.
The study on the metabolism after oral administration of chenodeoxycholic acid-24-14C was performed by analysis of radioactivity that had appeared in bile and feces of male hamsters. The radioactive bile acids
were analyzed by thin layer chromatography and identified by the isotope dilution method. In the bile of the hamsters with
bile fistula, radioactivity was originated from unchanged chenodeoxycholic acid for the most part, and 7-ketolithocholic acid,
lithocholic acid, and β-muricholic acid for the remainder. In the feces lithocholic acid, dehydrolithocholic acid, isolithocholic
acid, and unchanged form were identified. After the multiple dosing of chenodeoxycholic acid-24-14C for 6 days, β-muricholic acid was also identified in the feces. 相似文献
20.
Plasma cholesterol, arachidonic acid (AA, 20∶4n−6), and docosahexaenoic acid (DHA, 22∶6n−3) are higher in breast-fed infants
than in infants fed formula without cholesterol, AA, or DHA. This study investigated differences in plasma, hepatic, and bile
lipids and phospholipid fatty acids, and expression of hepatic proteins involved in sterol metabolism that result from feeding
formula with cholesterol with egg phospholipid to provide AA and DHA. For this study, three groups of piglets were evaluated:
piglets fed formula with 0.65 mmol/L cholesterol, the same formula with 0.8% AA and 0.2% DHA from egg phospholipid, and piglets
fed sow milk. Piglets fed the formula with phospholipid AA and DHA had higher plasma high density lipoprotein, but not apoprotein
(apo) B cholesterol or triglyceride; higher bile acid and phospholipid concentrations in bile; and higher liver and bile phospholipid
AA and DHA than piglets fed formula without AA and DHA (P<0.05). Hydroxy methylglutaryl (HMG)-CoA reductase and 7-α-hydroxylase, the rate-limiting enzymes of cholesterol and bile
acid synthesis, respectively, and low density lipoprotein receptor mRNA levels were not different between piglets fed formula
without and with phospholipid AA and DHA, but HMG-CoA reductase and 7α-hydroxylase mRNA were higher, and plasma apo B containing
lipoprotein cholesterol was lower in all piglets fed formula than in piglets fed milk. These studies show that supplementing
formula with AA and DHA from egg phospholipid alters bile metabolism by increasing the bile AA and DHA, and bile acid and
phospholipid. 相似文献