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Departments of Biochemistry and * Physiology, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, The People's Republic of China
2To 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: • cholesterol • Camellia sinensis • epicatechins • Mesocricetus auratus • triacylglycerols
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Neaton et al. 1984
). Tea is one of the most popular beverages in Chinese
society. There is an increasing interest in green tea as a protective
agent against cardiovascular disease (Chisaka et al. 1988
, Imai and Nakachi 1995
, Kono et al. 1992
). In this connection, several epidemiologic studies have
shown an inverse association between tea consumption and coronary heart
diseases (Hertog et al. 1993
, Stensvold et al. 1992
). In fact, increased consumption of green tea has been
associated with decreased serum triacylglycerols
(TG)3
and cholesterol (Kono et al. 1992
). The effect of
drinking green tea but not black tea on plasma lipoproteins appears to
be characterized by decreasing LDL cholesterol and increasing HDL
cholesterol (Green and Harari 1992
, Imai and Nakachi 1995
). This suggests that the beneficial effect of
drinking green tea over black tea is attributed to the content of green
tea epicatechins (GTE). In green tea, GTE remain relatively unchanged
compared with the fresh tea leaves, whereas in black tea, they are
degraded by the fermentation process during manufacture.
The GTE consists mainly of four derivatives; these include
(-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin
gallate (ECG) and (-)-epigallocatechin gallate (EGCG) (Fig. 1
). This study was designed to test the hypothesis that the GTE
derivatives are the major active compounds responsible for this
hypolipidemic activity; hamsters were used as an animal model. This was
done by comparing the hypolipidemic activity of green tea water extract
with that of isolated GTE from green tea. We also sought to determine
whether supplementation of GTE would lead to any changes in liver fatty
acid synthase (FAS), 3-hydroxy-3-methyl glutaryl coenzyme A redutase
(HMG-CoA-R), a key enzyme in cholesterol synthesis, and intestinal acyl
CoA:cholesterol acyltransferase (ACAT), which is believed to play an
important role in intestinal cholesteryl esterification before
cholesterol is absorbed and assembled in the chylomicrons.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The GTWE was prepared by adding 7.5 g jasmine tea (Camellia
sinensis) leaves to 500 mL of freshly boiled water (80°C).
After 15 min, the infusion was filtered and saved at 4°C until used
the next day. It was found that GTE in water was stable at least for
2 d (Zhu et al. 1997
).
Preparation of GTE extract.
Jasmine GTE was extracted and its individual derivatives were analyzed
by HPLC as previously described (Zhang et al. 1997a
). In
brief, 10 g of dry jasmine tea leaves were extracted three times
with 140 mL of hot distilled water (80°C). The infusion was then
cooled to room temperature, filtered and extracted with an equal volume
of chloroform to remove caffeine and pigments. The remaining aqueous
layer was then extracted twice with an equal volume of ethyl acetate.
The ethyl acetate containing GTE was then pooled and evaporated using a
vacuum rotary evaporator. The resulting GTE was then dissolved in 10 mL
of distilled water and freeze-dried overnight. Afterwards, a
portion of the extract was used to make a 5.0 g GTE/L solution.
The remaining dry GTE extract was then saved for supplementing the
diet.
The total GTE and individual derivatives in jasmine GTE extract were
analyzed as previously described (Zhang et al. 1997a
and
1997b). The total amount of GTE extracted varies with variety of teas,
methods used and different laboratories (Graham 1992
).
The extraction method used in this study yielded 75 g GTE/kg
jasmine green tea leaves with a purity of 95% in which EGCG, EGC, ECG
and EC accounted for 62.3, 19.2, 8.3 and 4.6%, respectively.
Animals.
Male Syrian golden hamsters (Mesocricetus auratus, The Chinese University of Hong Kong, Shatin, Hong Kong) were housed (2 hamsters/cage) in an animal room at 23°C with a 12-h light:dark cycle. Fresh semisynthetic diets were given to the animals daily, and uneaten food was discarded. Food intake was measured daily and body weight was recorded twice a week. The hamsters were given free access to food and fluid. The protocol was reviewed and approved by the Committee of Animal Ethics, The Chinese University of Hong Kong.
Diet.
The hypercholesterolemic diet described by Sanders and Sandaradura (1992)
was modified and used in this study. The
diet was high in fat and cholesterol and was prepared by mixing the
following ingredients: casein, 200 g; lard, 200 g;
cornstarch, 418 g; sucrose, 100 g; AIN-76 mineral mix,
40 g; AIN-76A vitamin mix, 20 g; DL-methionine,
1 g; and cholesterol, 1 g. The ingredients were purchased
from Harlan Teklad (Madison, WI) except for lard, which was obtained
from the local market, and DL-methionine and cholesterol,
which were purchased from Sigma Chemical (St. Louis, MO). For
Experiment 1, the hamsters were fed this hyperlipidemic diet with GTE
supplemented in the distilled water. For Experiments 2 and 3, the
GTE-supplemented diet was prepared by adding jasmine GTE extract to
this hyperlipidemic diet (powder form), which was then mixed with 1 L
gelatin solution (200 g/L). Once the gelatin had set, the food was cut
into ~20-g cubed portions and stored frozen at -20°C. For
Experiment 4, the hamsters were fed a nonpurified diet (Rodent Chow,
Purina Mills, St. Louis, MO); the GTE was added to distilled water.
Experiment 1.
The objective was to test the hypolipidemic effect of GTWE solution and the same amount of GTE extract dissolved in drinking water. Male hamsters (2 mo; 95–110 g,) were randomly divided into three groups (n = 12). They were fed the control diet containing no GTE as described above. One group of hamsters received the distilled water, whereas the other two groups received either 5.0 g GTE/L solution or 15 g GTWE/L solution as the only source of drinking water. For all three groups, sucrose was added to the fluid at the concentration of 15 g/L to overcome the bitterness of the green tea solutions. Freshly prepared solution was given and the intake was measured daily. At the end of 4 wk, all fluids were withdrawn and the distilled water was given instead. After food was withheld for 14 h, the hamsters were killed and blood was collected via the abdominal aorta. After clotting, the blood was centrifuged at 1300 x g for 10 min, and serum was then collected.
Experiment 2.
The objective was to examine the dose-dependent hypolipidemic activity of jasmine GTE extract supplemented in the diet. Male hamsters (2.5 mo, 125–140 g) were randomly divided into four groups (n = 9). All animals received the tap water as the only drinking fluid. One group of hamsters was fed the control diet, whereas the other three groups were given one of the three GTE-supplemented diets (1.1, 3.4 and 5.7 g GTE/kg). At the end of 4 wk, all of the hamsters were killed after food deprivation for 14 h. The blood was collected via the abdominal aorta and the serum was obtained as above.
Experiment 3.
The objective was to monitor the time-course changes in serum total
cholesterol (TC) and TG in hamsters given a GTE-supplemented diet.
In brief, male hamsters (2.5 mo, 125–140 g) were randomly divided into
two groups (n = 7). One group was fed the control
diet containing no GTE, whereas the other group was fed the same diet
supplemented with 5.7 g GTE/kg diet, a level previously shown to
significantly reduce serum TG and TC concentrations. All hamsters were
allowed free access to tap water. On d 2, 14 and 28, after food
deprivation for 14 h, the hamsters were bled from the
retro-orbital sinus into a heparinized capillary tube under light
ether anesthesia (Silverman 1987
). The total fecal
output of each cage was combined into two periods, d 0–20 and d
21–34, to determine total fecal fatty acids, neutral and acidic
sterols. At the end of 5 wk, after food deprivation for 14 h, the
hamsters were killed and blood was collected via the abdominal aorta.
The serum was collected and stored in aliquots at -76°C. The liver,
feces and carcass (whole body-perirenal adipose tissue-liver-blood)
was also retained to measure TG, phospholipids (PL) and free fatty
acids (FFA) according to the methods previously described (Chen et al. 1997
).
Experiment 4.
The objective was to measure the activity of HMG-CoA-R in the liver of hamsters fed low cholesterol nonpurified diet because high dietary cholesterol inhibits this enzyme. Male hamsters (2.5 mo, 125–140 g) were divided into two groups (n = 9) and fed the nonpurified diet. The control group was supplied distilled water, whereas the GTE group was given water containing 5.0 g GTE/L. For both the control and GTE-supplemented group, sucrose was added to the fluid at a concentration of 15g/L to overcome the bitterness of GTE. Hamsters were then killed by anesthesia under carbon dioxide and the liver was saved for the HMG-CoA-R assay. The intestine was also saved; the first 10 cm from the stomach was discarded, and the next 30 cm taken for the intestinal ACAT assay. Tissues were stored at -78°C for 6 wk.
Determination of blood cholesterol and apolipoproteins.
Several enzymatic kits were purchased from Sigma Chemical to measure
serum TG (#336–20), TC (#352–20), and HDL-cholesterol (HDL-C;
#352–4). Serum apolipoprotein A-1 (Apo A-1) and apolipoprotein B (Apo
B) were measured using Sigma commercial immunoassay kits (Apo B,
#357-A; Apo A-1, #356-A) as previously described by Rifai and King (1986)
.
Determination of liver cholesterol.
Total lipids were extracted from 300 mg of liver with the addition of stigmastanol (Sigma Chemical) as an internal standard using chloroform/methanol (2:1, v/v). The lipid extracts were then saponified with 6 mL of 1 mol/L NaOH in 90% ethanol at 90°C for 1 h, and the nonsaponified substances including cholesterol were converted to their trimethylsilyl (TMS)-ether derivatives by a commercial TMS reagent (Sigma). Analysis of the cholesterol TMS-ether derivative was performed in a fused silica capillary column (SAC-5, 30 m x 0.25 mm, i.d.; Supelco, Bellefonte, PA) using a Shimadzu GC-14 B gas-liquid chromatograph equipped with a flame ionization detector (Kyoto, Japan).
Determination of fecal neutral and acidic sterols.
Stigmasterol (0.3 mg) as an internal standard for neutral sterols was
added to a fecal sample (300 mg). The sample was then saponified using
9 mL of 1 mol/L NaOH in 90% ethanol containing 0.3 mg hyodeoxycholic
acid as an internal standard for acidic sterols (Sigma). The total
neutral sterols were extracted using 8 mL of cyclohexane and were then
converted to their corresponding TMS-ether derivatives for GLC
analysis. A typical chromatogram of the fecal neutral sterol profile is
illustrated in Figure 2
A.
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B. Assays of HMG-CoA-R, ACAT and FAS.
Liver micosomes were isolated according to Erickson et al. (1977)
. The activity of liver HMG-CoA-R was measured as
previously described by Shapiro et al. (1969)
and
modified by Heller and Strewsbury (1976)
. The activity
of liver FAS was measured using the methods described by
Nepokroeff et al. (1975)
. Mucosa microsomes were
prepared according to the method described by Murakami et al. (1995)
. The activity of intestinal ACAT was determined using
the method of Helgerud et al. (1981)
.
Statistics.
Data are expressed as means ± SD. For Experiments 1
and 4, both ANOVA and Student's t test (two-tailed)
were used where applicable for statistical evaluation of significant
differences between the control and the GTE-supplemented groups.
For Experiments 2 and 3, data were analyzed using a multivariate
procedure for repeated measurements as described previously
(Cole and Grizzle 1966
, LaTour and Miniard 1983
) using Sigmastat (Jandel Scientific Software, San Rafael,
CA). Differences were considered significant when P
< 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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No significant differences in body weight gain and food intake were
observed among the control, GTE and GTWE groups (Table 1). However, fluid consumption by the GTWE group was significantly
higher than that in the control and GTE groups (P < 0.01). The GTE and GTWE solutions used had similar concentrations of
total tea epicatechin derivatives (data not shown). Compared with the
control, serum TG, TC and Apo B were significantly lower in both the
GTE and GTWE groups (P < 0.05, Table 2). In contrast, the concentration of serum HDL-C and Apo A-1
did not differ among the three groups.
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No differences in body weight or food intake were found between the
control and the three groups supplemented with various levels of GTE in
the diet (Table 1)
. Significantly lower levels of serum TG and TC were
observed in all GTE-supplemented groups compared with those of the
control group (P < 0.05, Table 3). The hypolipidemic effects of dietary GTE were dose dependent
among the control, 3.4 and 5.7 g GTE/kg diet groups (P
< 0.05), although serum TG and TC did not differ in the 1.1 and
3.4 g GTE/kg diet groups. As in Experiment 1, dietary GTE did not
affect serum HDL-C.
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After 14 d of consumption of the high fat and cholesterol diet,
serum TG and TC levels were elevated in the controls and in hamsters
fed the 5.7 g GTE/kg diet (Fig. 3
). After 28 d, the differences between the control and
5.7 g GTE/kg diet groups were significant (P < 0.05) with the latter having lower serum TG and TC concentrations. At
the end of the experiment, serum TG was 35% (P < 0.05; Table 4) lower, whereas serum TC was 31% lower (P < 0.05; Table 4
) in the GTE-supplemented group compared with that of
the control group. After 5 wk, hamsters fed the 5.7 g GTE/kg diet
had significantly lower serum Apo B than controls, whereas Apo A-1
levels did not differ (Table 4)
. Thus, the ratio of Apo A-1 to Apo B
was greater in the GTE-supplemented group.
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5). In contrast, carcass and liver PL did not differ in the two
groups (data not shown). The carcass but not the livers of the
GTE-supplemented hamsters were characterized by a lower TG/FFA
ratio compared with that of the control group. Carcass fatty acid
composition did not differ in the control and the GTE-supplemented
groups except for oleic acid, which was lower in the latter (45.8 vs.
46.6% total fatty acids; P < 0.05). The activity of
liver FAS did not differ in the control and GTE-fed groups [8.2
± 1.6 vs. 8.3 ± 0.7 nmol/(min · mg protein)].
GTE-supplemented hamsters had higher fecal excretion of total neutral
sterols and cholesterol per se during the first 20 d of the
experiment compared with those fed the control diet (P
< 0.05, Table 6, Experiment 3). The output of total fecal bile acids in the
GTE-supplemented group was not different from that in the control
group during the first 20 d but it was greater (P
< 0.05) during d 21–34 (Table
7). Among the bile acids, deoxycholic acid and chenodeoxycholic acid
plus cholic acid were significantly higher in the feces of hamsters fed
the diet supplemented with GTE, whereas the concentration of
lithocholic acid did not differ between the groups.
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Experiment 4.
The activity of liver HMG-CoA-R in the hamsters drinking the fluid containing 5.0 g GTE/L [26.4 ± 2.8 pmol/(min · mg protein)] was not different from that of controls [27.3 ± 2.0 pmol/(min · mg protein)]. Similarly, no difference in the activity of intestinal ACAT existed between the control [171.9 ± 118.9 pmol/(min·mg protein)] and GTE groups [142.8 ± 69.6 pmol/(min · mg protein)].
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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,
Kono et al. 1992
). However, this is in contrast to two
other studies in which no correlation between tea consumption and
plasma cholesterol was found (Brown et al. 1993
,
Klatsky et al. 1985
). Japanese consume mainly green tea,
whereas Caucasians drink mainly black tea. The beneficial effect of
drinking green tea over black tea may be attributed to its higher
content of GTE for the following reason. In green tea, GTE remain
relatively unchanged compared with the fresh tea leaves, whereas in
black tea, they are mostly oxidized during the fermentation process
(Graham 1992
). This study demonstrated that jasmine GTWE
solution and the isolated GTE possessed similar hypolipidemic
activities (Table 2)
. This finding indicates that GTE are the major
active components or contribute at least in part to the hypolipidemic
activity of green tea.
A plausible mechanism for the hypocholesterolemic activity of GTE may
be its inhibition of cholesterol and bile acid absorption. This study
is the first report to examine the influence of dietary GTE on the
profile of both fecal neutral and acidic sterols. The excretion of
fecal neutral sterols (cholesterol and coprostanone) during d 0–20 and
acidic sterols (deoxycholic acid, chenodeoxycholic acid and cholic
acid) during d 21–34 were significantly greater in the
GTE-supplemented hamsters than in controls (Tables 2
and 3)
. The
observation that the excretion of bile acids was greater during d
21–34 but not during d 0–20 is unexplained. Perhaps the effect of the
diet change from the nonpurified diet to the hyperlipidemic diet on
fecal excretion of bile acids had not taken place during the first week
of the experiment. It also is unknown why fecal cholesterol in the
GTE-supplemented group was higher than that in the control group
only during d 0–20 but not during d 21–34. Perhaps the hamsters
adapted to the GTE, somehow compensating for its interference with
cholesterol absorption. Further study is therefore needed to examine
the effect of dietary GTE on both fecal neutral and acidic sterols on a
daily basis. Nevertheless, the reduced absorption of dietary
cholesterol during d 0–20 was directly associated with a lower serum
cholesterol concentration in the GTE-supplemented group. In
addition, the greater synthesis and excretion of acidic sterols (the
major end products of cholesterol catabolism) in hamsters fed GTE
during d 21–34 would also serve to lower the level of serum
cholesterol.
Cholesterol homeostasis is a delicate balance among dietary intake,
synthesis and catabolism. Serum total cholesterol can be lowered if
cholesterogenesis is inhibited. HMG-CoA-R mediates the first committed
step in the de novo synthesis of cholesterol from its precursor,
acetate. The partial inhibition of this rate-limiting enzyme by
dietary plant sterols and hypocholesterolemic drugs such as lovastin
and simvastatin is a typical example of reducing plasma cholesterol
(Brown and Goldstein 1986
). In this study, the activity
of HMG-CoA-R did not differ in the control and GTE-supplemented
hamsters, suggesting that inhibition of this enzyme is not part of the
hypocholesterolemic mechanism of GTE.
Intestinal ACAT plays a key role in the intestinal absorption of
cholesterol by esterifying cholesterol before its absorption
(Largis et al. 1989
, Wrenn et al. 1995
).
It has been shown that tea catechins decrease micellar solubility and
intestinal absorption of cholesterol in rats (Stensvold et al. 1992
). We hypothesized that GTE may interfere with the
absorption of cholesterol by inhibiting the ACAT activity. However,
dietary GTE had no influence on the intestinal ACAT activity,
suggesting that GTE increases the fecal output of cholesterol mainly as
a result of its binding capacity and acceleration of cholesterol
excretion. In fact, GTE has been shown to form insoluble coprecipitates
with cholesterol and thus decrease cholesterol absorption
(Muramatsu et al. 1986
).
This study also demonstrated that dietary GTE had TG-lowering
activity in hamsters. It is unlikely related to the inhibitory effect
on liver fatty acid synthesis because there was no difference in
hepatic FAS activity between the control and GTE-supplemented
groups. Most likely, the higher output of fecal fatty acids in the
GTE-supplemented group would be one of the possible mechanisms. It
should be pointed out that the concentrations of serum TG in the
control group of Experiments 1, 2 and 3 were inconsistent. We have no
clear explanation for this discrepancy, but the following factors my be
involved. First, the body weight gain and the food intake in
Experiments 2 and 3 were greater than those in Experiment 1. Thus, the
fat intake in Experiments 2 and 3 was greater than that in Experiment
1, resulting in a higher level of serum TG (Tables 2,
3
and 4)
. Second,
the diet in Experiment 1 was in the form of powder, whereas in
Experiments 2 and 3, the diet was set in gelatin. Third, the enzymatic
kit measuring serum TG in Experiment 1 was not from the same batch as
that used in Experiments 2 and 3, although both batches were purchased
from Sigma Chemical.
Jasmine GTE not only reduced serum TG and TC but also Apo B with
no effect on Apo A-1. Apo B is the principal protein in LDL, comprising
~90% of total LDL protein mass (Rifai 1986
). It plays
a major role in the recognition of cellular receptors for the
catabolism of LDL (Naito 1986
). Numerous studies have
indicated that Apo A-1 and Apo B measurements are useful in assessing
the risk of cardiovascular disease (Kottke et al. 1986
,
Maciejko et al. 1983
, Naito 1986
). It has
been reported that they are more specific and sensitive biochemical
markers of cardiovascular disease risk than HDL-C and LDL-C.
People with a low Apo A-1/Apo B ratio might have a higher risk of
cardiovascular disease (Kukita et al. 1984
). The present
results clearly demonstrated that supplementation of GTE in either diet
or drinking water modified favorably the balance of these two
apolipoproteins (Tables 2
and 4)
. If drinking green tea is associated
with a significantly lower risk of cardiovascular disease in humans,
part of the mechanism may involve an increase in Apo A-1/Apo B ratio.
Suppression of body TG accumulation in the GTE-supplemented group
was another major finding in this study (Table 5)
. First, greater
excretion in fecal total fatty acids (only during d 0–20 in Experiment
3) may contribute in part to a lower body TG accumulation in hamsters
supplemented with GTE. Second, dietary GTE may enhance the hydrolysis
of TG to FFA for oxidation. This was supported by the observation that
carcass FFA concentration was significantly higher in hamsters
supplemented with GTE (Table 5)
. This was also reflected in the
significantly lower TG/FFA ratio of GTE-fed hamsters. In fact, a
previous study by Sano et al. (1986)
demonstrated that
adrenaline-induced lipolytic activity in abdominal adipose tissue
was significantly elevated in rats given green tea for 8 or 16 wk. It
is unlikely that lower body TG accumulation in the GTE-supplemented
group was associated with suppression in fat synthesis because no
difference in the activity of liver FAS was observed between the
control and GTE-supplemented groups.
|
). The intake of 0.45, 1.34 and
2.33 g GTE/d would therefore correspond to drinking 3, 9 and 15
cups (100 mL/cup) of jasmine tea beverage daily, provided that each cup
of tea beverage contained 2 g of dry tea leaves. In fact, most
Chinese and Japanese tea drinkers usually consume >3 cups of tea per
day and some heavy drinkers may have >10 cups (1 L) each day
(Imai and Nakachi 1995
).
In addition to their hypolipidemic activities, GTE and its four major
epicatechin derivatives, EC, ECG, EGC and EGCG (Lunder 1992
), are believed to have a wide range of other
pharmaceutical properties including being antioxidative (Ding et al. 1992
, Miura et al. 1994
), anticarcinogenic
(Shi et al. 1994
) and antihypertensive (Henry and Stephens-Larson 1984
). We have previously shown that these
GTE derivatives exhibited stronger antioxidative effects than the
commercially available antioxidant, butylated hydroxytoluene, in foods
(Chen and Chan 1996
). It also has been demonstrated that
these compounds are more protective than ascorbate against
LDL-oxidation (Zhang et al. 1997a
). These GTE
derivatives protect not only 
-tocopherol but also docosahexaenoic
acid and arachidonic acid in LDL and red blood cell membranes from
oxidation (Zhang et al. 1997a and 1997b
). It has been
suggested that oxidative modification of LDL may play a role in the
development of atherosclerosis (Jialal and Devaraj 1996
). If tea consumption in humans is associated with a
significant decrease in cardiovascular disease, part of the mechanism
may also involve protection of LDL against oxidative modification in
addition to tea's hypolipidemic activity.
The high fat and cholesterol diet was used in this study to elevate serum TG and cholesterol to a level similar to that in humans. The present results in hamsters, although not directly applicable to humans, may have some implications for individuals who often consume a high fat and cholesterol diet. The reduction in serum TG and cholesterol by dietary GTE is not associated with inhibition of liver FAS, HMG-CoA-R and intestinal ACAT, but it is most likely mediated by its inhibition of absorption of dietary fat, cholesterol and reabsorption of bile acids.
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FOOTNOTES |
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3 Abbreviations used: ACAT, acyl CoA:cholesterol
acyltransferase; Apo A-1, apolipoprotein A-1; Apo B, apolipoprotein B;
EC, epicatechin; ECG, epicatechin gallate; EGC, epigallocatechin; EGCG,
epigallocatechin gallate; FAS, fatty acid synthase; FFA, free fatty
acids; GTE, green tea epicatechins; GTWE, green tea water extract;
HDL-C, high density lipoprotein cholesterol; HMG-CoA-R,
3-hydroxy-3-methyl glutaryl coenzyme A reductase; PL, phospholipids;
TC, total cholesterol; TG, triacylglycerols; TMS, trimethylsilyl.
Manuscript received August 3, 1998. Initial review completed October 15, 1998. Revision accepted February 23, 1999.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Brown C. A., Bolton-Smith C., Woodward M., Tunstall-Pedoe H. Coffee and tea consumption and the prevalence of coronary heart disease in men and women: results from the Scottish Heart Health Study. J. Epidemiol. Community Health 1993;47:171-175[Abstract]
2.
Brown M. S., Goldstein J. L. A receptor-mediated pathway for cholesterol homeostatsis. Science (Washington, DC) 1986;232:34-47
3. Chen Z. Y., Chan P. T. Antioxidative activity of green tea catechins in canola oil. Chem. Phys. Lipids 1996;82:163-172
4.
Chen Z. Y., Sea M. M., Kwan K. Y., Leung Y. H., Leung P. F. Depletion of linoleate induced by weight cycling is independent of extent of calorie restriction. Am. J. Physiol. 1997;272(Regul. Integr. Comp. Physiol. 41):R43-R50
5. Chisaka T., Matsuda H., Kubomura Y., Mochizuki M., Yamahara J., Fujimura H. The effect of crude drugs on experimental hypercholesterolemia: mode of action by (-) epigallocatechin gallate in tea leaves. Chem. Pharm. Bull 1988;36:227-233
6. Cole J.W.L., Grizzle J. Applications of multivariate analysis of variance to repeated measurements experiment. Biometrics 1966;22:810-828
7. Ding Z. Y., Chen Y., Zhou M., Fang Y. Z. Inhibitory effect of green tea polyphenol and morin on the oxidative modification of low-density lipoprotein. Chin. J. Pharmacol. Toxicol. 1992;6:263-266
8.
Erickson S. K., Cooper A. D., Matsui S. M., Gould R. G. 7-Ketocholesterol: its effects on hepatic cholesterogenesis and its hepatic metabolism in vivo and in vitro. J. Biol. Chem. 1977;252:5186-5193
9. Graham H. N. Green tea composition, consumption and polyphenol chemistry. Prev. Med. 1992;21:334-350[Medline]
10. Green M. S., Harari G. Association of serum lipoproteins and health-related habits with coffee and tea consumption in free-living subjects examined in the Israeli CORDIS study. Prev. Med. 1992;21:532-545[Medline]
11. Grundy S. M. Cholesterol and coronary heart disease: a new era. J. Am. Med. Assoc. 1986;256:2849-2858[Medline]
12. Heider J. G., Pickens G. E., Kelly L. A. Role of acyl CoA:cholesterol acyltransferase in cholesterol absorption and its inhibition by 57–118 in the rabbit. J. Lipid Res. 1983;24:1127-1134[Abstract]
13. Helgerud P., Saarem K., Norum K. R. Acyl-CoA:cholesterol acyltransferase in human small intestine: its activity and some properties of the enzymic reaction. J. Lipid Res. 1981;22:271-277[Abstract]
14.
Heller R. A., Strewsbury M. A. 3-Hydroxy-3-methylglutaryl coenzyme A reductase from rat liver. Its purification, properties and immunochemical study. J. Biol. Chem. 1976;251:3815-3822
15.
Henry J. P., Stephens-Larson P. Reduction of chronic psychosocial hypertension in mice by decaffeinated tea. Hypertension 1984;6:437-444
16. Hertog M. G., Feskens E. J., Hollman P. C., Katan M. B., Kromhout D. Dietary antioxidant flavonoids and risk of coronary heart disease: The Zutphen Elderly Study. Lancet 1993;342:1007-1011[Medline]
17.
Imai K., Nakachi K. Cross sectional study of effects of drinking green tea on cardiovascular and liver diseases. Br. Med. J. 1995;310:693-696
18.
Jialal I., Devaraj S. Low-density lipoprotein oxidation, antioxidants, and atherosclerosis: a clinical biochemistry perspective. Clin. Chem. 1996;42:498-506
19. Klatsky A. L., Petitti D. B., Armstrong M. A., Friedman G. D. Coffee, tea and cholesterol. Am. J. Cardiol. 1985;55:577-578[Medline]
20. Kono S., Shinchi K., Ikeda N., Yanai F., Imanishi K. Green tea consumption and serum lipid profiles: a cross-sectional study in Northern Kyushu, Japan. Prev. Med. 1992;21:526-531[Medline]
21. Kottke B. A., Zinsmeister A. R., Holmes D. R., Jr, Kneller R. W., Hallaway B. J., Mao S. J. Apolipoproteins and coronary artery disease. Mayo Clin. Proc. 1986;61:313-320[Medline]
22. Kukita H., Hiwada K., Kokubu T. Serum apolipoprotein A-I, A-II and B levels and their discriminative values in relatives of patients of coronary artery disease. Atherosclerosis 1984;51:261-267[Medline]
23. Largis E. E., Wang C. H., De Vries V. G., Schaffer S. A. CL 277,082: a novel inhibitor of ACAT-catalyzed cholesterol esterification and cholesterol absorption. J. Lipid Res. 1989;30:681-690[Abstract]
24. LaTour S. A., Miniard P. W. The misuse of repeated measures analysis in marketing research. J. Market Res. 1983;20:1399-1403
25. Lunder T. L. Catechins of green tea. Ho C.T. Lee C.Y. Huang M.T. eds. Phenolic Compounds in Food and Their Effects on Health II 1992:114-120 American Chemical Society Washington, DC.
26. Maciejko J. J., Homes D. R., Kottke B. A., Zinsmeister A. R., Dinh D. M., Mao S. J. Apolipoprotein A-1 as a marker of angiographically assessed coronary artery disease. N. Engl. J. Med. 1983;309:385-389[Abstract]
27. Miura S., Watanabe J., Tomita T., Sano M., Tomita I. The inhibitory effects of tea polyphenol (flava-3-ol derivatives) on Cu++-mediated oxidative modification of low density lipoprotein. Biol. Pharm. Bull. 1994;17:1567-1572[Medline]
28. Murakami S., Araki H., Otomo S., Nara Y., Yamori Y. Effects of HL-004: a novel ACAT inhibitor, on cholesterol accumulation and removal in cultured smooth muscle cells from stroke-prone spontaneously hypertensive rats (SHRSP). Life Sci 1995;56:509-520[Medline]
29. Muramatsu K., Fukuyo M., Hara Y. Effect of green tea catechins on plasma cholesterol level in cholesterol-fed rats. J. Nutr. Sci. Vitaminol. 1986;32:613-622
30. Naito H. K. The clinical significance of apolipoprotein measurements. J. Clin. Immunoass. 1986;9:11
31. Neaton J. D., Kuller L. H., Wentworth D., Borhani N. O. Total and cardiovascular mortality in relation to cigarette smoking, serum cholesterol concentration and diastolic blood pressure among black and white males followed up for five years. Am. Heart J. 1984;108:759-769[Medline]
32. Nepokroeff C. M., Lakshmanan M. R., Porter J. W. Fatty acid synthase from rat liver. Methods Enzymol 1975;35:37-44[Medline]
33. Rifai N. Lipoproteins and apolipoproteins: composition, metabolism, and association with coronary heart diseases. Arch. Pathol. Lab. Med. 1986;110:694-701[Medline]
34.
Rifai N., King M. E. Immunoturbidimetric assays of apolipoproteins A, A-1, A-2 and B in serum. Clin. Chem. 1986;32:957-958
35. Sanders T. A., Sandaradura S. The cholesterol-raising effect of coffee in the Syrian hamster. Br. J. Nutr. 1992;68:431-434[Medline]
36. Sano M., Takenaka Y., Kojima R., Saito S., Tomita I., Katou M., Shibuya S. Effects of Pu-Erh tea on lipid metabolism in rats. Chem. Pharm. Bull. 1986;34:221-228
37. Shapiro D. J., Imblum R. L., Rodwell V. W. Thin-layer chromatographic assay for HMG-CoA reductase and mevalonic acid. Anal. Biochem. 1969;31:383-390[Medline]
38.
Shi S. T., Wang Z. Y., Smith T. J., Hong J. Y., Chen W. F., Ho C. T., Yang C. S. Effects of green tea and black tea on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone bioactivation: DNA methylation and lung tumorigenesis in A/J mice. Cancer Res 1994;54:4641-4647
39. Silverman J. Biomethodology. Van Hoosier G.I. McPherson C.W. eds. Laboratory Hamsters 1987:69-93 Academic Press Toronto, Canada.
40. Stensvold I., Tverdal A., Solvoll K., Foss D. P. Tea consumption: relationship to cholesterol, blood pressure, and coronary and total mortality. Prev. Med. 1992;21:546-553[Medline]
41. Wrenn S. M., Parks J. S., Jr, Immermann F. W., Rudel L. L. ACAT inhibitors CL283,546 and CL283,796 reduce LDL cholesterol without affecting cholesterol absorption in African green monkeys. J. Lipid Res. 1995;36:1199-1210[Abstract]
42. Zhang A., Chan P. T., Luk Y. S., Ho W.K., K & Chen Z. Y. Inhibitory effect of jasmine green tea epicatechin isomers on LDL-oxidation. J. Nutr. Biochem. 1997;8:334-340
43. Zhang A., Zhu Q. Y., Luk Y. S., Ho K. Y., Fung K. P., Chen Z. Y. Inhibitory effects of jasmine green tea epicatechin isomers on free-radical-induced lysis of red blood cells. Life Sci 1997;61:383-394[Medline]
44. Zhu Q. Y., Zhang A., Tsang D., Huang Y., Chen Z. Y. Stability of green tea catechins. J. Agric. Food Chem. 1997;45:4624-4628
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