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Ben May Institute for Cancer Research, Department of Biochemistry and Molecular Biology, and Tang Center for Herbal Medicine Research, University of Chicago, Chicago, Illinois 60637
Address all correspondence and requests for reprints to: Dr. S. Liao, Ben May Institute for Cancer Research, University of Chicago, 5841 South Maryland Avenue, MC 6027, Chicago, Illinois 60637. E-mail: sliao{at}huggins.bsd.uchicago.edu
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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We reported previously that ip injection of (-)-epigallocatechin
gallate (EGCG), one of the major green tea catechins (Fig. 1
), can within 7 days rapidly suppress
human prostate and breast tumor growth in athymic mice (14). To assess
possible physiological effects of green tea consumption, we studied the
acute effects of EGCG on endocrine systems.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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In vivo treatment
EGCG and other catechins (>98% pure) were isolated from green
tea (Camellia sinensis) in our laboratory as described
previously (6). Catechins were dissolved in water for oral
administration and in sterile PBS for ip injection. Rats in control
groups received vehicle only. Testosterone propionate (TP) and
5
-dihydrotestosterone propionate (DHTP) were dissolved in sesame
oil, and 4 mg in 0.5 ml sesame oil (16 mg/kg BW) were injected sc daily
when indicated.
Food-restricted, male Sprague Dawley rats were given 12 g rat chow daily, which was about 50% of the amount consumed daily by each control rat. The body weight and the amount of food and water consumed were monitored daily. Food consumption was monitored in rats caged in groups of three to five animals by weighing food pellets every 24 h. On the final day, rats were anesthetized with methoxyflurane, and blood was collected by heart puncture. Sera were collected after centrifugation (10,000 x g for 20 min at 4 C) for biochemical analysis.
Biochemical analysis
For biochemical analysis, commercially available RIA kits for
insulin-like growth factor I (IGF-I) and testosterone
(Diagnostics Systems Laboratories, Inc., Webster, TX), LH
and GH (Amersham Pharmacia Biotech, Arlington Heights,
IL), leptin and insulin (Linco Research, Inc., St.
Charles, MO), and corticosterone (ICN Biomedicals, Inc.,
Costa Mesa, CA) and analytical kits for glycerol and triglyceride
(Sigma, St. Louis, MO) and fatty acids (Roche Molecular Biochemicals, Indianapolis, IN) were used. Proximate
composition analysis of rats was performed by COVANCE Laboratory
(Madison, WI). Complete blood count and serum chemistry
(e.g. cholesterols, glucose, and enzymatic activities) were
determined by the Animal Resource Center at the University of
Chicago.
Statistical analysis
Data are expressed as the mean ± SEM. Unpaired
Student’s t test was used to examine differences between
control and the EGCG-injected groups. ANOVA and Student-Newman-Keuls
multiple range test were used to examine differences among various
groups. P < 0.05 indicated significance.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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), caused
acute body weight loss in Sprague Dawley male (Figs. 2A and 3A) and female (Fig. 4A) rats
within 2–7 days of treatment. In male Sprague Dawley rats, the effect
of EGCG on body weight was dose dependent (Fig. 2). Doses of 5 or 10 mg
EGCG (26 and 53 mg/kg BW) injected daily were not effective or were
less effective in reducing the body weight than 15 mg (
85 mg/kg BW).
Male Sprague Dawley rats injected daily ip with 26 and 53 mg EGCG/kg BW
gained body weight by 17–24% relative to their initial body weight,
but lost 5–9% relative to the control animals after 7 days of
treatment (Fig. 2A). Male Sprague Dawley rats daily injected ip with 85
mg EGCG/kg BW lost 15–21% of their body weight relative to their
initial weight and 30–41% relative to the control weight after 7 days
of treatment (Figs. 2A and 3A and Table 1). Control rats continued growth and
increased their body weight by 25–34% relative to their initial
weight (Figs. 2A, 3A, and 4A and Table 1). Female Sprague Dawley rats
injected daily ip with 12.5 mg EGCG (92 mg/kg BW) lost 10% of their
body weight relative to their initial weight and 29% relative to the
control weight after 7 days of treatment (Fig. 4A). Therefore, an EGCG
dose of 70–92 mg/kg BW was used in most experiments.
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, B–F) on the weight of accessory
sexual organs was also observed. The weights of androgen-sensitive
organs, such as ventral (Fig. 2C) and dorsolateral (Fig. 2D) prostates,
seminal vesicles (Fig. 2E), coagulating glands (Fig. 2F), and preputial
glands (Fig. 2F) were reduced by 50–70% after 7 days of treatment
with EGCG (85 mg/kg BW). Weight changes in these sexual organs were
modulated in a catechin-specific manner (Fig. 3, C–F). Relative to control animals
killed at the start of the experiment, these accessory sexual organs
(except preputial gland) in male Sprague Dawley rats were reduced by
30–50% in weight after 7 days of EGCG treatment (Fig. 2, B–F).
Similarly, the weights of estrogen-sensitive organs, such as the uterus
(Fig. 4C) and ovary (Fig. 4D), in female
Sprague Dawley rats were reduced by about 50% after 7 days of EGCG
treatment. The weights of liver and kidney were also decreased by about
20% (data not shown). In male Sprague Dawley and lean Zucker rats
treated with EGCG for 7–8 days, the weights of the liver, kidney, and
testis were reduced by about 10–20%, whereas spleen weight was
reduced by about 15–30% (Table 1). However, there was no change in
these organ weights from those in male obese Zucker rats treated with
EGCG for 4 days (Table 1).
Sex hormones, leptin, IGF-I, insulin, LH, and GH
Rats treated with EGCG had significant changes in various
endocrine parameters. After 7 days of treatment with EGCG (85 mg/kg
BW) circulating testosterone (Fig. 3B and Table 1) was reduced by about
70% in male Sprague Dawley rats. Similarly, the circulating level of
17ß-estradiol was reduced by 34% (Fig. 4B) in females after 7 days
of EGCG treatment. In both male and female Sprague Dawley rats, 7 days
of EGCG treatment caused significant reduction in blood levels of
leptin, IGF-I, and insulin (Fig. 5, A–D,
and Table 1). Dose-dependent effects of EGCG in male Sprague Dawley
rats were also observed on levels of serum testosterone, leptin, IGF-I,
and insulin (Fig. 5A). With male and female Sprague Dawley rats treated
with EGCG for 7 days, we also observed that the serum level of LH was
significantly reduced (40–50%; Fig. 5E), whereas that of GH was
increased in males or reduced in females (Fig. 5F). However, the
pulsatile nature of GH secretion prevented us from making definite
conclusions about changes in circulating levels of GH in these rats.
The effects of EGCG on sex hormones and various peptide hormones
investigated was not mimicked by other structurally similar catechins
(i.e. ECG with one less hydroxyl group than EGCG was not
active; Fig. 5).
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). For both Sprague Dawley and
Zucker rats, significant effects were observed with 70–92 mg EGCG/kg
BW.
Exogenous androgen reverses the effect of EGCG on accessory sexual
organs
To determine whether the reduction in weight of accessory sexual
organs was due to an EGCG-induced reduction in androgen levels, we
injected male Sprague Dawley rats with androgen and/or EGCG. We found
that EGCG did not cause prostate weight loss in male rats injected
daily with TP or DHTP (Fig. 6A);
therefore, the EGCG effect on prostate weight was most likely secondary
to the EGCG-induced reduction in the level of testosterone in these
male rats. However, androgen administration was not able to prevent the
EGCG-induced body weight loss (Fig. 6B); food intake restriction (Fig. 7E); decreases in circulating leptin
(Fig. 6D), IGF-I (Fig. 6E), insulin (Fig. 6F), and LH (Fig. 6G); or
increase in circulating GH (Fig. 6H).
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). Similar changes in these serum
nutrients were observed in male lean and obese Zucker rats. Proximate
composition analysis of animals showed that Sprague Dawley rats treated
daily with EGCG for 7 days had no change in percent water and protein
content, a moderate decrease in carbohydrate content (2.5% in control
and 1.3% in the EGCG-treated group), but a very large reduction in fat
content (from 4.1% in controls to 1.4% in the EGCG-treated group).
Within 7–8 days, EGCG treatment decreased sc fat by 40–70% and
abdominal fat by 20–35%, but not epididymal fat, in male Sprague
Dawley and lean Zucker rats (Table 2). A 20% loss of abdominal fat was
seen in obese male Zucker rats within 4 days of EGCG treatment (Table 2).
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, A and B)
and female (Fig. 7C) rats consumed about 50–60% less food than
control rats. Similar effects of EGCG on food intake were observed with
obese male Zucker rats (Fig. 7D). Therefore, body weight loss was due
to reduced intake of food. As food restriction can alter hypothalamic
function and decrease the level of LH and sex steroids (16, 17), we
restricted the food intake of Sprague Dawley male rats (not injected
with EGCG) by about 50% for 7 days and found that the blood level of
testosterone was indeed reduced by about 60% and ventral prostate
weight was decreased by about 50% compared with those in animals given
free access to food (Table 3). Serum
leptin, IGF-I, insulin, LH, and GH were also decreased after food
restriction. Administration of androgen to male Sprague Dawley rats was
not able to prevent the EGCG-induced food intake reduction (Fig. 7E).
These effects of EGCG, administered ip, were diminished or absent when
EGCG was administered orally (Table 3).
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and 5). Neither EGCG nor structurally related
ECG caused significant changes in the serum levels of total protein,
albumin, blood urea nitrogen, creatine,
PO43-,
Na+, K+,
Ca2+, Cl-, and enzymes
that are indicative of severe damage to liver and other organs, such as
lactate dehydrogenase, alanine aminotransferase, aspartate
aminotransferase, and 
-glutamyltranspeptidase (Table 4). However,
significant changes in the amount of blood bilirubin and the activity
of blood alkaline phosphatase were observed. In blood of rats treated
with EGCG, red blood cell and hemoglobin concentrations increased by
about 20%, whereas the concentrations of white blood cells,
lymphocytes, and monocytes decreased about 10%, 31%, and 24%,
respectively (Table 5). Both eosinophil and platelet concentrations
increased by 100%.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The effects of EGCG on body weight loss, hormone level changes, and food intake depend on the route of administration. The effects of EGCG were not observed or were less when the same amount of EGCG was given to rats orally for 7 days. This may be due to inefficient absorption of EGCG (13, 18, 19) and suggests that the effects of EGCG administered ip were not caused by interaction of EGCG with food or by EGCG action inside the gastrointestinal tract.
We have determined the plasma concentration of EGCG by HPLC (20) and have also found that after ip injection of Sprague Dawley rats with 100 mg EGCG/kg BW, plasma EGCG levels were 24, 2, 4, 1, and 1 µM at 0.5, 1, 2, 5, and 24 h, respectively (average of three rats). Therefore, EGCG may have systemic effects in this study. A plasma EGCG concentration of 1 µM would be similar to levels in humans (70 kg) 1 h after drinking 6–12 cups (200 ml/cup) of tea (18).
The biological effects of EGCG have often been attributed to its in vitro effects on different enzyme activities (4, 5, 6), cell proliferation (9, 10, 11), and transcriptional activators (1) as well as its antioxidant and free radical-scavenging activity (7, 8). The effects of EGCG on various endocrine parameters that we have observed may be explained as secondary effects of EGCG on food intake. For example, the large decrease in circulating leptin in EGCG-treated rats could have been caused by diminished fat stores due to low food intake in these rats. Both glucose and insulin stimulate leptin gene expression (21, 22); therefore, low circulating levels of glucose and insulin, possibly resulting from low food intake, may also have contributed to the effect of EGCG on the leptin level. However, other mechanisms for the effects of EGCG, besides lowering food intake, should be explored.
The effect of EGCG, but not those of other related catechins, on food intake is interesting. A 50% decrease in food intake was seen by the second day of treatment with 80 mg EGCG/kg BW. The EGCG effect on food intake was not dependent on an intact leptin receptor, as the leptin receptor-defective obese Zucker rats also responded to EGCG. EGCG may interact specifically with a component of a leptin receptor-independent appetite control pathway and reduce food intake. As food intake is regulated by a variety of peripheral factors and by central neuroendocrine systems (23, 24), we measured plasma levels of peptides, such as ACTH, neuropeptide Y, CRF, urocortin, and galanin, in male Sprague Dawley rats after they were treated with 83 mg EGCG/kg BW for 2 days. EGCG did not change plasma levels of these neuropeptides (our unpublished observations). Whether hypothalamic neuropeptide gene expression is altered by EGCG is being investigated. Various hormones, including cholecystokinin, glucagon-like polypeptide-1, glucagon, substance P, somatostatin, and bombesin, have been reported to inhibit food intake (23, 24). Further study is required to determine whether any of these components is responsible for the effect of EGCG on food intake.
EGCG does not appear to be toxic to the liver and kidney, as 1) EGCG
did not cause significant changes in the serum level of total protein,
albumin, blood urea nitrogen, creatine,
PO43-,
Na+, K+,
Ca2+, Cl-, and enzymes
that are indicative of severe damage to liver and other organs; 2) EGCG
had no effect on male Sprague Dawley rat liver ornithine decarboxylase
activity (an indicator of cell proliferation that increases upon liver
damage) (25); and 3) in lean and obese Zucker rats, we did not observe
any visible differences between microscopic histology of the liver and
kidney of EGCG-treated rats and those of the controls. Although no
statistically significant elevation of serum aspartate
aminotransferase and -glutamyltranspeptidase activity
was observed in EGCG-treated rats, the small increase in the activities
of these enzymes in serum may be indicative of an effect of EGCG on
liver or may be related to lowered food intake (26). Significant
changes in serum bilirubin and alkaline phosphatase activity in
EGCG-injected rats may also be related to diet restriction (26, 27).
Although detailed toxicological studies of EGCG have not been reported,
a condensed polyphenol structurally related to EGCG, procyanidin B-2,
has a lethal dose greater than 2000 mg/kg BW when sc injected into rats
(28).
Although oral administration of EGCG was not effective within 7–14 days, long term oral consumption of green tea or EGCG-containing extracts may mimic some of the acute EGCG effects described in this report and may be beneficial to health. Studies have shown that oral consumption of green tea or EGCG can lower rat and human serum cholesterol levels (29, 30, 31), increase rat high density lipoprotein cholesterol (30), decrease rat and human low density lipoprotein cholesterol (30, 31), and lower rat blood glucose (32) and triglyceride (30). Based on oral and ip effects of EGCG on serum hormones and nutrients, long term consumption of green tea may influence the incidence of obesity, diabetes, and cardiovascular disease. Recently, it was shown that EGCG inhibits angiogenesis (33), which may relate to the effects of EGCG on tumor growth (14). Also, by lowering plasma levels of sex steroids and other endocrine factors, such as IGF-I, long term use of EGCG or green tea may be effective in the prevention and suppression of the growth of hormone-dependent and -independent prostate and breast cancer (14, 34, 35). This may relate to the low occurrence of breast and prostate cancer metastasis and mortality in some Asian countries (14, 36) where green tea is consumed regularly. Despite many potential benefits of green tea and EGCG consumption, it is also important to evaluate undesirable health-related consequences that may arise from EGCG- induced reductions in the levels of sex steroid hormones and other endocrine factors.
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Acknowledgments |
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Footnotes |
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2 These authors contributed equally to this work.
Received October 7, 1999.
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References |
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-reductase isozymes by tea epicatechin-3-gallate and
epigallocatechin-3-gallate. Biochem Biophys Res Commun 214:833–838[CrossRef][Medline]
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), EC (
), EGC (
), ECG (
), and EGCG (•) groups.
), DHTP (
) groups.