![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
*
School of Food and Nutritional Sciences, The University of Shizuoka, Shizuoka 422-8526, Japan and
Department of Applied Biological Sciences, Nagoya University, Nagoya 464-8601, Japan
2To whom correspondence and reprint requests should be addressed.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
-hydroxylase
(CYP7A1) activity and its mRNA level increased significantly, and the
supplementation of taurine further enhanced these indexes, indicating
an increase in cholesterol degradation. The abundance of mRNA for Apo
A-I, one of the main components of HDL, was reduced by HC and
recovered by taurine supplementation. Agarose gel electrophoresis
revealed that, in hypercholesterolemic rats fed the HC diet, the serum
level of the heavier VLDL increased significantly, but taurine
repressed this increase and normalized this pattern. Significant
correlations were observed between the time- and dose-dependent
increases of CYP7A1 gene expression and the decrease of blood
cholesterol concentration in rats fed the HC diet supplemented with
taurine (time, r = -0.538, P
< 0.01, n = 32; dose, r = -0.738, P < 0.001, n = 20).
These results suggest that the hypocholesterolemic effects of taurine
observed in the hypocholesterolemic rats fed the HC diet were mainly
due to the enhancement of cholesterol degradation and the excretion of
bile acid.
KEY WORDS: • taurine • cholesterol • hypocholesterolemia • cholesterol 7-hydroxylase (CYP7A1) • rat
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
, Wright et al. 1986
). Suggested biological and physiological functions of
taurine include cell membrane stabilization (Pasantes-Morales et al. 1985
), antioxidation (Nakamura et al. 1933
),
detoxification (Huxtable 1992
), osmoregulation
(Thurston et al. 1980
), neuromodulation (Bernardi 1985
, Kuriyama 1980
) and brain and retinal
development (Sturman 1986
). Taurine is an essential
nutrient for cats (Hayes et al. 1975
), and
formula-fed, preterm infants are unable to maintain normal plasma
and urinary taurine levels, although no functional impairment has been
reported (Raiha et al. 1975
). In lipid metabolism, the
function of taurine is considered only because of its conjugation with
bile acids in the liver (Danielsson 1963
), which
increase the use of bile acids, the degrading metabolites of
cholesterol and that participate in the formation of micelles that are
used for fat absorption in the small intestine (Yamanaka et al. 1986
). Numerous studies have been done that sought the effect
of taurine on cholesterol metabolism (Cantafora et al. 1986
, Gandhi et al. 1992
, Herrmann 1959
, Murakami et al. 1996
, Petty et al. 1990
, Sugiyama et al. 1989
, Yan et al. 1993
) in various species, including rats, guinea pigs, rabbits
and cats, and almost all of the experiments have been conducted in
animals with hypercholesterolemia induced by feeding a
high-cholesterol diet. We also reported a hypocholesterolemic
action of taurine in rats fed a high-cholesterol diet
(Nanami et al. 1996
), but the mechanism of its action is
unclear. In rats fed a high cholesterol diet, cholesterol balance is
dependent on the catabolism of cholesterol because cholesterol
synthesis is abolished in these rats. Taurine is used for bile acid
conjugation and may facilitate bile acids excretion in feces. Moreover,
taurine itself may enhance the biotransformation of cholesterol to bile
acids, and then increased bile acids might enhance the clearance of
cholesterol out of the body. Therefore, we examined the
hypocholesterolemic action of taurine by focusing on the degradation of
circulating cholesterol.
In the present study, we examined the mechanisms of the
taurine-induced reduction of serum cholesterol in
hypercholesterolemic rats fed a high-cholesterol diet. We studied
the degradation of cholesterol, which is associated with cholesterol 7
-hydroxylase
(CYP7A1)3
.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Young male Wistar rats, weighing about 100 g (Japan SLC,
Hamamatsu), were maintained at 24°C with a 12-h light (0700–1900 h)
and dark cycle. To accustom the rats to the experimental conditions,
they were initially given free access to a 20% casein diet (control
diet) for 2 d before being divided into groups. The compositions
of the test diets are shown in Table 1
. Animals were fed the control diet, a taurine-supplemented diet, a
high-cholesterol (HC) diet, or a HC diet supplemented with various
levels of taurine (HCT) for 2 wk. The HC diet contained 10 g
cholesterol and 2.5 g sodium cholate per kg diet. Taurine was added, at
various levels, to the control diet at the expense of carbohydrate.
Rats were individually housed in stainless steel cages in a room with
controlled temperature (23°C) and humidity (55%) and were given free
access to the experimental diets and water. The experimental procedures
used in this study met the guidelines of the Animal Care and Use
Committee of the University of Shizuoka.
|
The dose-dependent effect of taurine on hypocholesterolemia was examined in three experiments (experiments 1, 2 and 6). In expt. 1, 54 rats were divided into nine groups (six rats per group) and were provided with the control diet, the HC diet or HCT diet (0.25, 0.5, 10, 20, 30, 40 or 50 g taurine/kg diet) for 2 wk. In expt. 2, 42 rats were divided into seven groups and were provided with the control diet, the HC diet or the HCT diet (0.5, 1, 2.5, 5 or 10 g taurine/kg diet) for 2 wk. In both experiments 1 and 2, animals were killed between 1100–1300 h on the last day of the experimental period.
The effects of taurine on the serum and liver lipids, cholesterol degradation and lipoprotein distribution were examined in experiments 3 and 4. In both experiments, rats were fed one of the following diets for 2 wk: control diet, taurine-supplemented diet (50 g taurine/kg control diet), HC diet, or HCT diet (50 g taurine/kg HC). In experiment 3, we determined the concentrations of serum and liver lipids and the amount of fecal steroid excretion as assessed by cholesterol and bile acids in the feces. In experiment 4, we examined the serum lipoprotein distribution and determined the mRNA level of CYP7A1, the rate-limiting enzyme in the metabolic pathway of cholesterol to bile acids. Animals were killed at ~1100 h. In experiment 5, animals were killed at 1100 h and 0100 h to examine the effects of taurine on the activity and mRNA level of CYP7A1. In experiment 6, the correlation between serum total cholesterol concentration and the level of CYP7A1 mRNA was also determined. In this experiment, animals were fed the HC diet or the HCT diets (5, 10, 30 or 50 g taurine/kg diet) for 2 wk and were killed at 0100 h to measure the hepatic levels of CYP7A1 mRNA. Blood was collected from a cervical wound, and tissues were immediately removed, frozen in liquid nitrogen and stored at -80°C until assayed.
Biochemical analyses.
Serum and tissues (liver, kidney and heart) were deproteinized by using
sulfosalicilic acid, and taurine concentrations in these tissues were
measured with an automatic amino acid analyzer (Model L-8500; Hitachi,
Tokyo). Serum lipids (total cholesterol, HDL-cholesterol,
triglycerides and phospholipids) were determined by using commercial
kits (Cholesterol C-test, HDL-cholesterol-test, Triglyceride
G-test and Phospholipids B-test, respectively; Wako Pure
Chemical, Osaka,). About 2 g of liver were homogenized, and lipids
were extracted with a chloroform:methanol mixture (2:1. v/v) as
described by Folch et al. (1957)
. Total lipids in the liver were
determined gravimetrically. The concentration of liver cholesterol in
the lipid extracts was measured enzymatically by using a kit
(Cholesterol C-test; Wako Pure Chemical). Hepatic triglyceride
concentration was determined by the acetyl acetone method
(Fletcher 1968
). The amount of hepatic phospholipids was
calculated by subtracting the amount of liver cholesterol and
triglycerides from the total lipid contents. The concentration of
reduced glutathione in the liver was determined by using Ellman's
reagent (Sedlak and Lindsay 1968
). Fecal bile acids were
extracted by the mixture of chloroform and methanol (1:1, v/v) and were
determined enzymatically by the method of Sheltawy and Losowsky (1975)
.
The activity of CYP7A1 was determined as described previously
(Oda et al. 1989
). In brief, the liver microsome was
incubated in the reaction buffer containing 100 mmol potassium
phosphate/L (pH 7.4), 0.1 mmol EDTA/L, 50 mmol NaF/L, 2 mmol NADPH/L,
20 mmol cysteamine/L, 0.2 mmol cholesterol/L, 1.5g Tween 80/L, 222 kBq
[7-3H] cholesterol. After the termination of the
reaction with trichloroacetic acid, the supernatant fraction was
extracted with chloroform two times. The radioactivity of the upper,
aqueous phase was counted with a liquid scintillation counter (Aloka,
Tokyo). Total RNA was isolated according to the method described by
Chomczynski and Sacchi (1987)
, and 10 µg of total RNA was subjected
to Northern blot hybridization. The cDNA clones of rat apolipoprotein
(apo) A-I (Boguski et al. 1985
), rat CYP7A1
(Noshiro et al. 1989
), and mouse apo E (Horiuchi et al. 1989
) were labeled with Megaprime DNA labeling system
(Amersham, Tokyo) and used for hybridizations. Specific hybridization
was quantified with an image analyzer (BAS 2000, Fuji Film, Tokyo). The
apo E mRNA level was not affected by any treatment employed in this
study (data not shown), so we used it as a normalization standard
(Oda et al. 1995
, Yoshida et al. 1996
),
Agarose gel electrophoresis of serum lipoproteins.
Agarose gel electrophoresis was carried out by using Corning Universal Film from Corning (Palo Alto, CA). After the agarose gel was running at 90 V for 1 h, lipoprotein-cholesterol was stained with Co-Cholest-A (Nippon Chemiphar, Tokyo).
Statistics.
The means and SEM of 4–8 rats per group are reported. In
experiments 1, 2 and 6, significance of differences among values was
analyzed by one-way ANOVA. When treatment was significant,
Duncan's multiple range test was performed (Duncan 1955
). In experiments 3–5, significance of differences among
values was analyzed by two-way ANOVA (Oda et al. 1991
). When interaction was significant, Student's
t-test was performed (Snedecor and Cochran 1967
). P values of < 0.05 were considered
significance. All statistical analyses were performed using the
Statistical Analysis System (SAS/STAT Version 6, SAS Institute, Cary,
NC).
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Body weight gain and food intake of rats fed the HCT diet (0.25, 0.5,
10, 20, 30, 40 and 50 g taurine/kg diet) did not differ from those
of rats fed the control or HC diets (Table 2
; experiment 1). The animals fed the HC diet showed a significantly
higher serum total cholesterol than those fed the control diet, but the
supplementation of 0.25 g taurine/kg diet significantly reduced
the concentration of serum total cholesterol in a dose-dependent
manner. The extent of the reduction of serum cholesterol induced by
dietary taurine reached a plateau at the level of 10 g taurine/kg
diet. Serum HDL-cholesterol was significantly reduced by feeding
the HC diet, and the supplementation of taurine significantly and
dose-dependently suppressed this reduction. The maximal effect of
taurine on the restoration of serum HDL-cholesterol was obtained at
the level of 10 g taurine/kg diet. Because there was a big
difference in the hypocholesterolemic effect between dietary levels of
0.5 and 10 g taurine/kg diet, in experiment 2, intermediate levels
of taurine, i.e., 0.5, 1, 2.5, 5 and 10 g/kg diet, were supplemented to
the HC diet (Table 3
; expt. 2). The hypercholesterolemia induced by feeding the HC diet was
gradually and dose-dependently reduced by the supplementation of
taurine, and its reduction was significant at the level of 1 g
taurine /kg diet supplemented to the diet. In animals fed the diet
containing 2.5 g taurine /kg diet, serum total cholesterol was
recovered to the normal level (Table 3)
.
|
|
Taurine concentrations in the liver and the kidney were significantly
and dramatically decreased by feeding the HC diet, and taurine
supplementation significantly increased the taurine concentrations in
the liver (at 10 g taurine/kg) and the kidney (at >0.05 g
taurine/kg) (Table 4
; expt. 1). The effects of taurine supplementation on the tissue taurine
concentrations of rats fed the HC diet were determined in more detail
in experiment 2. The decreased level of serum taurine concentration
caused by the intake of the HC diet was gradually restored by the
administration of taurine in a dose-dependent manner. Similar
elevation of the taurine concentration was obtained in the liver and
the heart in animals fed the HCT diet. Serum, liver, and heart taurine
concentrations that were not less than those of controls were found in
rats fed 2.5 g taurine/kg diet.
|
Body weight gain and food intake of rats did not differ among the
groups, in spite of taurine supplementation (Table 5
). Liver weight of rats fed the HC diet was significantly greater than
that of rats fed the control diet, and taurine supplementation
significantly suppressed this increase of liver weight. Differences in
serum cholesterol of rats fed the HC or HCT diets were almost the same
as in the previous experiments 1 and 2. Dietary taurine significantly
reduced the serum triglyceride concentration in rats fed either the
control or the HC diet. Taurine tended to decrease the concentration of
serum phospholipids in rats fed the HC diet. The concentrations of the
lipids, such as cholesterol, triglyceride, phospholipids as well as
total lipids were unaltered in the liver of rats fed the
taurine-supplemented, control diet. The concentrations of these
lipids in the liver were significantly elevated by feeding the HC diet,
and dietary taurine significantly reduced the extent of this increase
in these hepatic lipids, even in the rats fed the HC diet. The
concentration of reduced glutathione in the liver was significantly
increased by the supplementation of taurine in rats fed either the
control or the HC diet. The excretion of fecal cholesterol was
significantly greater in rats fed the HC diet than in those fed the
control diet. Taurine significantly enhanced the excretion of bile
acids in rats fed the HC diet, but not in rats fed the control diet. In
expt. 4, serum lipids were affected by taurine in the same manner as in
expt. 3 (Table 5)
. The concentrations of hepatic mRNA of CYP7A1 were
increased significantly by feeding the HC diet, and further increase in
the CYP7A1 mRNA level was seen in rats fed the HCT diet.
|
In the hypercholesterolemic rats fed the HC diet, pre-ß lipoprotein
cholesterol markedly increased (Fig. 1
). The pre-ß lipoprotein migrated somewhat slowly like ß-VLDL
(Mahley et al. 1980
). The addition of taurine to the HC
diet drastically repressed the increase in the amount of VLDL
cholesterol and thus normalized the lipoprotein profile. These results
indicate that dietary taurine specifically reduces the molecular form
of VLDL that was increased in quantity by feeding the HC diet.
|
The activity and mRNA of CYP7A1 in the liver are known to exhibit a
diurnal rhythm, and the highest level is observed during the dark
period (Noshiro et al. 1990
). We showed that CYP7A1 mRNA
in the liver was induced by dietary taurine when rats were killed
during the light period (Table 5)
. In experiment 5, we investigated the
effect of taurine on the activity and mRNA level of CYP7A1 in the liver
during both the light period (daytime) and the dark period (nighttime).
As shown above, the increase in the serum cholesterol induced by the HC
diet was completely abolished by dietary taurine during both the light
and dark periods (Fig. 2
A), and the cholesterol-lowering effect of taurine was more explicit
during the dark period. Both the activity and mRNA of CYP7A1 during the
dark period were higher than those during the light period (Fig. 2B
and
C). During both periods, dietary taurine increased the
activity and mRNA level of CYP7A1, and the variations of the activity
of CYP7A1 were in parallel with those of the level of CYP7A1 mRNA. The
highest activity and mRNA level of CYP7A1 were observed in HCT group
during the dark period, the group that showed the lowest level of serum
cholesterol. There was a significant negative correlation between serum
level of cholesterol and the mRNA level (Fig. 2D
, P < 0.01) and activity of CYP7A1 (P < 0.05, data not
shown).
|
In experiment 5 (Fig. 2)
, when the highest activity and mRNA of CYP7A1
was observed in the liver, the lowest level of serum cholesterol was
seen. This and the results in Table 5
led us to consider that the
increased CYP7A1 in the liver caused by taurine would stimulate the
excretion of steroids in the feces, and that it might be one of the
major reasons for the hypocholesterolemic action of taurine. To
determine the relationship between the serum cholesterol level and the
CYP7A1 gene expression in the liver, we again examined the
dose-dependent effect of dietary taurine in rats fed a HC diet.
Animals were killed during the dark period (0100 h). As shown in Table 2
, serum level of cholesterol was decreased by dietary taurine
(Fig. 3
A). The CYP7A1 mRNA level in the liver was increased by taurine in a
dose-dependent manner (Fig. 3A)
. Serum level of cholesterol had a
significant negative correlation with the hepatic CYP7A1 mRNA level (r
= 0.738, P < 0.001, Fig. 3B
).
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
). Tsuji et al. (1980)
also
reported that taurine had a hypocholesterolemic effect in
experimentally induced hypercholesterolemic animal models. However, the
mechanism of the hypocholesterolemic action of taurine was not clear.
In this study, we examined the hypocholesterolemic action of taurine by
focusing on the changes in dose-dependency, time-dependency,
distribution of lipoproteins and the degradation of circulating
cholesterol. Hypercholesterolemia caused by feeding the HC diet was
significantly restored by the supplementation of taurine in a
dose-dependent manner. That is, increased serum cholesterol caused
by feeding the HC diet was significantly decreased to the control value
by supplementation with only 2.5g taurine/kg diet. The supplementation
of 10 g taurine/kg diet normalized the concentrations of serum
HDL-cholesterol reduced by the HC diet. According to the agarose
gel electrophoresis (Fig. 1)
, the density of the band, which represents
mainly HDL-cholesterol, was significantly reduced, while heavier
VLDL fractions were remarkably enriched by feeding the HC diet. Also
the contents of hepatic mRNA of Apo A-I, one of the main component
of HDL, decreased in rats fed the HC diet. However, taurine
supplementation to the HC diet normalized it. Taurine concentrations
were reduced by the HC diet in various tissues, but they were recovered
by the supplementation of taurine; the dietary level of taurine
required for restoration of taurine was dependent on the tissues. From
the overall results, we conducted that the effective amount of taurine
to normalize serum cholesterol and tissue taurine concentrations is
around 1%. The degradation products of cholesterol are bile acids, and the conjugates of bile acids with taurine or glycine contribute in the solubilization and excretion of cholesterol. There is a species difference in the conjugation of bile acids, and in rats, the conjugates with taurine predominate. When rats were fed the HC diet, fecal excretion of cholesterol and bile acids increased significantly compared to those of rats fed the test diet without cholesterol, and taurine further increased the bile acids excretion. We found that, in the HC diet group, the content of hepatic mRNA of CYP7A1 significantly increased, and it was also further elevated by taurine.
It was reported that the supplementation of taurine increased the
activity of hepatic microsomal CYP7A1 in hamsters (Bellentani et al. 1987
) and guinea pigs (Kibe et al. 1980
).
This increase of microsomal CYP7A1 activity might indicate that taurine
promotes the conjugation of bile acids with taurine, leading to a
reduction of the concentration of serum cholesterol increased by
feeding the HC diet. Sugiyama et al. (1989)
reported that taurine
increased the activity of CYP7A1 in rats fed a HC diet, but glycine
administration did not alter this enzyme activity, in spite of the
reduction of serum cholesterol. Spady et al. (1995)
demonstrated that
the overexpression of exogenous CYP7A1 genes effectively reduced the
plasma level of cholesterol in hamsters fed a low- or high-fat,
western diet. There is a diurnal rhythm in the activity and mRNA of
CYP7A1 (Noshiro et al. 1990
). Therefore, in the next
experiments, to elucidate the relationship between serum level of
cholesterol and CYP7A1, time- and dose-dependent effects of dietary
taurine on serum cholesterol and CYP7A1 were investigated in rats fed
the HC diet. As shown in Figs. 2
and 3
, supplementation of taurine
reduced the blood level of cholesterol and induced CYP7A1 activity and
CYP7A1 gene expression. Moreover, serum cholesterol level was
negatively correlated with the CYP7A1 mRNA level. Our results presented
in this paper suggest that dietary taurine has a strong
hypocholesterolemic action through the induction of CYP7A1 gene
expression. Stephan et al. (1987)
demonstrated that taurine enhanced
LDL receptor activity in HepG2 cells. Although lipoprotein receptor
activity was not determined in this study, the increased catabolism of
cholesterol might result in enhancement of VLDL uptake in the liver
from serum.
The addition of taurine to the diet did not reduce serum level of
cholesterol in control rats (Table 4
and Fig. 2
) (Mochizuki et al. 1998
). Even in these rats fed a control diet, CYP7A1 was
induced by taurine (Fig. 2)
. We speculated that the loss of steroid
induced caused by taurine would be compensated for by the synthesis of
cholesterol. We thought that this would explain why hypocholesterolemic
action of taurine observed only in rats fed the HC diet.
There is no information as to how CYP7A1 gene expression is induced by
dietary taurine, so far. The CYP7A1 mRNA and protein levels are
regulated principally at the transcriptional level. Lavery and Schibler (1993)
observed a close correlation between the CYP7A1 transcription
rate and the level of D larger binding protein (DBP), one of the
liver-enriched transcription factors. It can be speculated that
there is a putative taurine responsive element in CYP7A1 genes.
However, there are some technical problems in investigating the effect
of taurine on CYP7A1 gene expression. Hepatoma cell lines and even
primary hepatocytes lose some liver-specific functions and normal
regulation of some gene expression. It was reported that CYP7A1 gene
expression was rapidly lost in primary cultured hepatocytes after
disaggregation (Hylemon et al. 1992
). We recently
demonstrated that CYP7A1 mRNA was maintained in hepatocytes cultured on
EHS-gel (Oda et al. 1997
). We are now investigating
how taurine regulates CYP7A1 gene expression on a molecular level. The
alternative possibility that enhancement of steroid excretion in feces
by taurine indirectly induce CYP7A1 gene expression should be examined.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
3 Abbreviations used: CYP7A1, cholesterol 7
-hydroxylase; HC, high-cholesterol diet; HCT,
high-cholesterol diet supplemented with taurine; apo,
apolipoprotein; DBP, D layer binding protein.
Manuscript received June 26, 1998. Initial review completed August 16, 1998. Revision accepted May 17, 1999.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. American Institute of Nutrition Report of the American Institute of Nutrition ad hoc committee on standards for nutritional studies. J. Nutr. 1977;107:1340-1348
2. Bellentani S., Pecorari M., Cordoma P., Marchegiano P., Manenti F., Bosisio E., De Fabiani E., Galli G. Taurine increases bile acid pool size and reduces bile saturation index in the hamster. J. Lipid Res. 1987;28:1021-1027[Abstract]
3. Bernardi N. On the role of taurine in the cerebellar cortex: A reappraisal. Acta Physiol. Pharmacol. Ther. Latinoam. 1985;35:153-164
4.
Boguski M. S., Elshoubagy N., Taylar J. M., Gordon J. I. Comparative analysis of repeated sequences in rat apolipoproteins A-I, A-IV, and E. Proc. Natl. Acad. Sci. USA 1985;82:992-996
5. Cantafora A., Mantovani A., Masella R., Mechelli L., Alvaro D. Effect of taurine administration on liver lipids in guinea pig. Experientia 1986;42:407-408[Medline]
6. Chesney R. W. Taurine: Its biological role and clinical implications. Adv. Pediatr. 1985;32:1-42[Medline]
7. Chomczynski P., Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal. Biochem. 1987;162:156-159[Medline]
8. Danielsson H. Present states of research on catabolism and excretion of cholesterol. Adv. Lipid Res. 1963;1:335-385[Medline]
9. Duncan D. B. Multiple range and multiple F tests. Biometrics 1955;11:1-42
10. Fletcher M. J. A colorimetric method for estimating serum triglycerides. Clin. Chim. Acta 1968;22:393-397[Medline]
11.
Folch J., Lees M., Sloane-Stanley G. H. A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chem. 1957;226:497-509
12. Gandhi V. M., Cherian K. M., Mulky M. J. Hypolipidemic action of taurine in rats. Ind. J. Exp. Biol. 1992;30:413-417[Medline]
13.
Hayes K. C., Carey R. E., Schmidt S. Y. Retinal degeneration associated with taurine deficiency in the cat. Science 1975;188:949-951
14.
Herrmann R. G. Effect of taurine, glycine and sitosterols on serum and tissue cholesterol in the rat and rabbit. Circ. Res. 1959;7:224-227
15.
Horiuchi K., Tajima S., Menju M., Yamamoto A. Structure and expression of mouse apolipoprotein E gene. J. Biochem. 1989;106:98-103
16.
Huxtable R. J. Physiological actions of taurine. Physiol. Rev. 1992;72:101-163
17.
Hylemon P. B., Gurley E. C., Stravitz R. T., Litz J. S., Pandak K. M., Chiang J.Y.L., Vlahcevic Z. R. Hormonal regulation of cholesterol 7 -hydroxylase mRNA levels and transcriptional activity in primary rat hepatocyte cultures. J. Biol. Chem. 1992;267:16866-16871
18. Kibe A., Wake C., Kuramoto T., Hoshita T. Effect of dietary taurine on bile acid metabolism in guinea pigs. Lipids 1980;15:224-229[Medline]
19. Kuriyama K. Taurine as a neuromodulator. Fed. Proc. 1980;39:2680-2684[Medline]
20.
Lavery D. J., Schibler U. Circadian transcription of the cholesterol 7 -hydroxylase gene may involve the liver-enriched bZIP protein DBP. Genes Dev 1993;7:1871-1884
21. Mahley R. W., Innerarity T. L., Brown M. S., Ho Y. K., Goldstein J. L. Cholesteryl ester synthesis in macrophages: Stimulation by ß-VLDL from cholesterol-fed animals of several species. J. Lipid Res. 1980;21:970-980[Abstract]
22. Mochizuki H., Oda H., Yokogoshi H. Increasing effect of dietary taurine on the serum HDL-cholesterol concentration in rats. Biosci. Biotechnol Biochem. 1998;62:578-579[Medline]
23. Murakami S., Nara Y., Yamori Y. Taurine accelerates the regression of hypercholesterolemia in stroke-prone spontaneously hypertensive rats. Life Sci 1996;58:1643-1651[Medline]
24. Nakamura T., Ogasawara M., Nemoto M., Yoshida T. The protective effect of taurine on the biomembrane against damage produced by oxygen radicals. Biol. Pharm. Bull. 1993;16:970-972[Medline]
25. Nanami K., Oda H., Yokogoshi H. Antihypercholesterolemic action of taurine on streptozotocin-diabetic rats or on rats fed a high cholesterol diet. Adv. Exp. Med. Biol. 1996;403:561-568[Medline]
26.
Noshiro M., Nishimoto M., Morohashi K., Okuda K. Molecular cloning of cDNA for cholesterol 7 -hydroxylase from rat liver microsomes. Nucleotide sequence and expression. FEBS Lett 1989;257:97-100[Medline]
27.
Noshiro M., Nishimoto M., Okuda K. Rat liver cholesterol 7 -hydroxylase: Pretranslational regulation for circadian rhythm. J. Biol. Chem. 1990;265:10036-10041
28. Oda H., Fukui H., Hitomi Y., Yoshida A. Alternation of serum lipoprotein metabolism by polychlorinated biphenyls and methionine in rats fed a soybean protein diet. J. Nutr. 1991;121:925-933
29. Oda H., Nozawa K., Hitomi Y., Kakinuma A. Laminin-rich extracellular matrix maintains high level of hepatocyte nuclear factor 4 in rat hepatocyte culture. Biochem. Biophys. Res. Commun. 1995;212:800-805[Medline]
30. Oda H., Nozawa K., Miyachi F., Shimizu A., Iwasaki Y., Kakinuma A. High responsiveness to thyroid hormone of adult rat primary hepatocytes cultured on EHS-gel. Biosci. Biotechnol. Biochem. 1997;61:1590-1592[Medline]
31. Oda H., Okumura Y., Hitomi Y., Ozaki K., Nagaoka N., Yoshida A. Effect of dietary methionine and polychlorinated biphenyls on cholesterol metabolism in rats fed a diet containing soy protein isolate. J. Nutr. Sci. Vitam. 1989;35:333-348
32. Pasantes-Morales H., Wright C. E., Gaull G. E. Taurine protection of lymphoblastoid cells from iron-ascorbate-induced damage. Biochem. Pharmacol. 1985;34:2205-2207[Medline]
33. Petty M. A., Kintz J., DiFracesco G. F. The effects of taurine on atherosclerosis development in cholesterol-fed rabbits. Eur. J. Pharmacol. 1990;180:119-127[Medline]
34. Raiha N., Rassin D., Heinonen K., Gaull G. E. Milk protein quality and quantity: Biochemical and growth effects in low birth weight infants (LBWI). Peddiatr. Res. 1975;9:370
35. Reeves P. G., Nielssen F. H., Fahey G. C. AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet. J. Nutr. 1993;123:1939-1951
36. Sedlak J., Lindsay R. H. Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissues with Ellman's reagent. Anal. Biochem. 1968;25:192-205[Medline]
37. Sheltawy M. J., Losowsky M. S. Determination of fecal bile acids by an enzymic method. Clin. Chim. Acta 1975;64:127-132[Medline]
38. Snedecor G. W., Cochran W. G. Statistical Methods 6th ed. 1967 Iowa State University Press Ames, IA.
39.
Spady D. K., Cuthbert J. A., Willard M. N., Meidell R. S. Adenovirus-mediated transfer of a gene encoding cholesterol 7 -hydroxylase into hamsters increases hepatic enzyme activity and reduces plasma total and low density lipoprotein (LDL) cholesterol. J. Clin. Invest. 1995;96:700-709
40.
Stephan Z. F., Lindsey S., Hayes K. C. Taurine enhances LDL binding: Internalization and degradation by cultured HepG2 cells. J. Biol. Chem. 1987;262:6069-6073
41. Sturman J. A. Nutritional taurine and central nervous system development. Ann. NY Acad. Sci. 1986;477:196-213[Medline]
42. Sugiyama K., Ohishi A., Ohnuma Y., Muramatsu K. Comparison between the plasma cholesterol-lowering effects of glycine and taurine in rats fed on high cholesterol diet. Agric. Biol. Chem. 1989;53:1647-1652
43. Thurston J. H., Hauhart R. E., Dirgo J. A. Taurine: A role in osmotic regulation of mammalian brain and possible clinical significance. Life Sci 1980;26:1561-1568[Medline]
44. Tsuji K., Iwao H., Nakagawa Y., Seki T. Influence of dietary taurine on distribution and fecal excretion of cholesterol in hypercholesterolemic rats. Sulfur-Containing Amino Acids 1980;3:165-171
45. Wright C. E., Tallan H. H., Lin Y. Y., Gaull G. E. Taurine: Biological update. Ann. Rev. Biochem. 1986;55:427-453[Medline]
46. Yamanaka Y., Tsuji K., Ichikawa T. Stimulation of chenodeoxycholic acid excretion in hypercholesterolemic mice by dietary taurine. J. Nutr. Sci. Vitaminol 1986;32:287-296
47. Yan C. C., Bravo E., Cantafora A. Effect of taurine levels on liver lipid metabolism: an in vivo study in the rat. Proc. Soc. Exp. Biol. Med. 1993;202:88-96[Medline]
48. Yoshida Y., Kimura N., Oda H., Kakinuma A. Insulin suppresses the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes. Biochem. Biophys. Res. Commun. 1996;229:182-188[Medline]
This article has been cited by other articles:
|
|
 |
|
  M. Hiroyama, T. Aoyagi, Y. Fujiwara, J. Birumachi, Y. Shigematsu, K. Kiwaki, R. Tasaki, F. Endo, and A. Tanoue Hypermetabolism of Fat in V1a Vasopressin Receptor Knockout Mice Mol. Endocrinol., January 1, 2007; 21(1): 247 - 258. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Tsuboyama-Kasaoka, C. Shozawa, K. Sano, Y. Kamei, S. Kasaoka, Y. Hosokawa, and O. Ezaki Taurine (2-Aminoethanesulfonic Acid) Deficiency Creates a Vicious Circle Promoting Obesity Endocrinology, July 1, 2006; 147(7): 3276 - 3284. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Oda Functions of Sulfur-Containing Amino Acids in Lipid Metabolism J. Nutr., June 1, 2006; 136(6): 1666S - 1669S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Kishida, S. Miyazato, H. Ogawa, and K. Ebihara Taurine Prevents Hypercholesterolemia in Ovariectomized Rats Fed Corn Oil but Not in Those Fed Coconut Oil J. Nutr., August 1, 2003; 133(8): 2616 - 2621. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. J. Sanchez-Muniz, M. C. Garcia-Linares, M. T. Garcia-Arias, S. Bastida, and J. Viejo Fat and Protein from Olive Oil-Fried Sardines Interact to Normalize Serum Lipoproteins and Reduce Liver Lipids in Hypercholesterolemic Rats J. Nutr., July 1, 2003; 133(7): 2302 - 2308. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Dorgru-Abbasoglu, O Kanbagli, J Balkan, U Cevikbas, G Aykac-Tokerl, and M Uysall The protective effect of taurine against thioacetamide hepatotoxicity of rats Human and Experimental Toxicology, January 1, 2001; 20(1): 23 - 27. [Abstract] [PDF]
|
|
|
|
 |
|
 J. Férézou, M. Combettes-Souverain, M. Souidi, J. L. Smith, N. Boehler, F. Milliat, E. Eckhardt, G. Blanchard, M. Riottot, C. Sérougne, et al. Cholesterol, bile acid, and lipoprotein metabolism in two strains of hamster, one resistant, the other sensitive (LPN) to sucrose-induced cholelithiasis J. Lipid Res., December 1, 2000; 41(12): 2042 - 2054. [Abstract] [Full Text]
|
|
|
|
|
|
H. Mochizuki, H. Oda, and H. Yokogoshi Dietary Taurine Alters Ascorbic Acid Metabolism in Rats Fed Diets Containing Polychlorinated Biphenyls J. Nutr., April 1, 2000; 130(4): 873 - 876. [Abstract] [Full Text]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
) and serum cholesterol level (•). Because the results of the
one-way ANOVA were significant (P < 0.05),
Duncan's multiple range test was performed. Values are means and
SEM for four rats in each point. Points with different
letters are significantly different (P < 0.05, uppercase letters
for serum cholesterol, lowercase letters for CYP7A1 mRNA). The values
of CYP7A1 mRNA in rats fed HC diet without taurine was set to 1.
(B): Relationships between hepatic level of CYP7A1 mRNA
and serum level of cholesterol in rats fed HC diet. The values of
CYP7A1 mRNA in rats fed HC diet without taurine was set to 1.