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Research Article
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Different Lipolytic Response to (-)-Epigallocatechin-3-gallate in Adipocytes Derived
from Normal Diet-fed Rats and High Fat Diet-fed Rats
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Pawitra Pulbutr,
Atika Jaruchotikamol,
Jirawan Chaiyachart,
Pannee Sonrasee
and
Wannaporn Poungpan
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ABSTRACT
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(-)-Epigallocatechin-3-gallate (EGCG), the major catechins
found in green tea, has been known to possess various pharmacological activities.
It has been demonstrated that EGCG affects on several adipocyte functions, involving
in its weight-controlling action. This study was aimed to investigate the effects
of EGCG on adipocyte lipolysis in adipocytes derived from Normal Pellet Diet
(NPD)-fed rats and High Fat Diet (HFD)-fed rats. Sixteen male Wistar rats were
divided into 2 groups (8 rats per group). The rats in each group were fed with
NPD or HFD for 3 weeks. The adipocyte suspensions were prepared by the collagenase
digestion method. The concentration of Free Fatty Acid (FFA) was measured after
1 h-incubation as an index of adipocyte lipolysis. EGCG at every concentration
tested (1, 5 and 10 μM) significantly stimulated basal lipolysis in adipocytes
derived from the NPD-fed rats with the FFA concentrations of 453.67±25.57,
458.87±26.84 and 443.97±19.75 μM mL-1 Packed Cell
Volume (PCV)/h, respectively (p<0.05). In adipocytes derived from the HFD-fed
rat, EGCG only at the concentration of 5 μM significantly increased basal
adipocyte lipolysis with the FFA concentration of 1,091.75±220.56 μM
mL-1 PCV h-1 (p<0.05; n = 4). Conversely, EGCG at any
of the concentrations tested did not cause a significant change in isoprenaline
(0.1 μM)-induced lipolysis in both adipocyte groups. These results indicate
a lower lipolytic action of EGCG in adipocytes derived from the HFD-fed rats.
Further experiments thus should be done to explore the reason for the difference
in the lipolytic response to EGCG between these adipocytes.
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How
to cite this article:
Pawitra Pulbutr, Atika Jaruchotikamol, Jirawan Chaiyachart, Pannee Sonrasee and Wannaporn Poungpan, 2012. Different Lipolytic Response to (-)-Epigallocatechin-3-gallate in Adipocytes Derived
from Normal Diet-fed Rats and High Fat Diet-fed Rats. Journal of Biological Sciences, 12: 294-300. DOI: 10.3923/jbs.2012.294.300 URL: https://scialert.net/abstract/?doi=jbs.2012.294.300
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Received: June 07, 2012;
Accepted: July 24, 2012;
Published: September 06, 2012
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INTRODUCTION
Obesity which is now considered as a global public health problem, has significant
impacts on various aspects, including physical and mental health, quality of
life and also economy (Luppino et al., 2010;
Cash et al., 2011; Von Lengerke
and Krauth, 2011). Although, obesity is a multifactorial disease, over food
consumption and lack of physical activity are known as the major causes of the
disease (Biro and Wien, 2010). Obesity is an established
risk factor for several chronic disorders such as hypertension, dyslipidemia,
type 2 diabetes and some forms of cancers (Kopelman, 2000).
Thus, prevention of obesity is the plausibly effective way to protect people
from aforementioned diseases. Adipocyte lipolysis which is characterized by
hydrolysis of triglyceride storage in adipocytes, plays a crucial role in the
regulation of fat mass (Arner, 2005). Modulation of
adipocyte lipolysis thus provides a potential way to reduce fat mass and alleviate
obesity and related disorders.
Since there are some limitations of conventional weight controlling programs,
pharmacologically active compounds derived from plants have been highly focused
as an alternative means to manage obesity. One of the most promising compounds
is green tea-derived (-)-epigallocatechin-3-gallate (EGCG). Green tea which
is obtained from the leaves of Camellia sinensis, is a widely consumed
oriental beverage. EGCG accounts for approximately 50% of the total amount of
catechins found in green tea (Balentine et al., 1997).
EGCG has been found to play a key role in various health-related benefits of
green tea, including its weight controlling action (Lee
et al., 2009a; Thielecke and Boschmann, 2009;
Chen et al., 2011). EGCG has been reported to
reduce fat mass by controlling various adipocyte functions, including suppression
of adipogenesis, inhibition of adipocyte lipogenesis and stimulation of adipocyte
lipolysis (Chan et al., 2011; Sung
et al., 2010; Lee et al., 2009a; Ogasawara
et al., 2011). However, the lipolytic effect of EGCG has not been
established in adipocytes derived from animals fed with high fat diet which
is a well-known model of diet-induced obesity. This study was aimed to investigate
the effects of EGCG on adipocyte lipolysis in isolated adipocytes derived from
high fat diet-fed rats and to compare its actions to those found in adipocytes
derived from normal diet-fed rats.
MATERIALS AND METHODS
Preparation of adipocytes: Sixteen male Wistar rats weighing 150-170
g were obtained from the National Laboratory Animal Center, Mahidol University,
Thailand. The animals were kept at constant temperature (25±1°C)
with a 12 h dark-light cycle. After acclimatization period of one week, the
rats were randomly divided into two groups. The rats in the first group (n =
8) were fed with Normal Pellet Diet (NPD) (C.P. mice feed food No. 082, Bangkok,
Thailand) (NPD-group), whilst the rats in the second group (n = 8) were fed
with high fat diet (HFD-group). The fat content in NPD and HFD are approximately
12 and 56% of total energy, respectively. High fat diet was prepared according
to the formulation of Srinivasan et al. (2005)
with slight modification. The animals were fed ad libitum and freely
accessed to water. After three weeks, the rats were sacrificed by CO2
overdose and epididymal fat pads were dissected for preparation of adipocyte
suspension. All procedures performed with the animals were approved by the animal
research ethic committee, Mahasarakham University, Thailand.
Adipocytes were isolated according to the method of Rodbell
(1964) with some modifications. Briefly, the epididymal fat pads were rinsed
with Hanks buffer containing 5 mM glucose and 0.5% bovine serum albumin (Sigma)
(BSA, with less than 0.005% (w/w) free fatty acid). Hanks physiological solution
containing (in mM): 5.6 KCl, 138 NaCl, 4.2 NaHCO3, 1.2 NaH2PO4,
2.6 CaCl2, 1.2 MgCl2, 10 HEPES, pH 7.4 (with NaOH). The
tissues were cut into small pieces and then digested with 0.25 mg mL-1
collagenase type II enzyme (Sigma) at 37°C. Isolated adipocytes were filtered
through nylon mesh and then rinsed twice with collagenase free Hanks buffer.
After the second wash, the adipocytes were resuspended with Hanks solution into
1:1 (v/v) proportion to give a final volume of the cell suspension at about
8-15 mL, depending on the volume of adipocytes. The cell suspension was transferred
to a fresh Nalgene conical flask and stored in the water bath at 37°C before
performing experiments. All experiments were conducted at the Faculty of Pharmacy,
Mahasarakham University, Thailand during 18th November 2011- 25th December 2011.
Adipocyte lipolysis: Adipocytes were incubated for 60 min in microcentrifuge
tubes at 37°C with Hanks buffer, pH 7.4, containing 5 mM glucose, 0.5% BSA
and various concentrations of (-)-Epigallocatechin-3-gallate (EGCG) (Sigma)
at 1, 5 and 10 μM. For stimulated lipolysis study, the experiments were
performed in the presence of isoprenaline (Sigma) at the concentration of 0.1
μM. The final volume of the incubations was adjusted to 1 mL. After 1 h
incubation, the cell free incubation media were collected and the concentrations
of Free Fatty Acid (FFA) were measured by using non-esterified fatty acid assay
kit from WAKO Chemicals (Japan).
Statistical analysis: The results are expressed as Mean±SEM.
Statistical analysis was performed by using either independent-sample Students
t-test or one-way analysis of variance (ANOVA) followed by Bonferroni post
hoc test. Statistical tests were performed using SPSS software version 16.0
(SPSS Inc., Chicago, Illinois, USA). The data was considered as significantly
different when p-value<0.05.
RESULTS
Body weight and epididymal fat pad weight: The body weight of the rats
was measured at the beginning of the experiment (day 0) and every week thereafter
(day 7, 14, 21 and 28). The body weight of the rats fed with NPD was not different
from that of the rats fed with HFD (Table 1). However, the
epididymal fat pad weight of the HFD-fed rats (2.03±0.13 g/100 g of body
weight, n = 8) was significantly higher than that of the NPD-fed control rats
(1.48±0.85 g/100 g of body weight, n = 8) with the p-value of <0.05
(Table 2).
Lipolytic effects of EGCG in adipocytes derived from the NPD-fed rats (NPD-group):
At the basal condition, the FFA concentration derived from adipocytes in the
NPD group was 323.46±28.32 μM mL-1 PCV h-1
(Fig. 1).
Table 1: |
Body weight of NPD-fed rats and HFD-fed rats |
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Values are Mean±SEM, n = 8, There is no statistically
significant difference between groups. The statistical analysis was performed
by using independent-sample Students t-test |
Table 2: |
Weight of epididymal fat pads of NPD-fed rats and HFD-fed
rats |
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*p<0.05 when compared with the NPD group (independent-sample
Students t-test), Values are Mean±SEM, n = 8 |
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Fig. 1: |
Basal lipolysis and isoprenaline (0.1 μM)-induced lipolysis
in adipocytes derived from the NPD-group and the HFD-group. The results
are expressed as the Mean±SEM (n = 5). *p<0.05 when compared with
basal lipolysis in the NPD group; #p<0.05 when compared with
basal lipolysis in the HFD group (independent-sample Students t-test) |
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Fig. 2: |
Effects of EGCG on basal adipocyte lipolysis in the NPD-group.
The results are expressed as the Mean±SEM (n = 5). *p<0.05 when
compared with basal lipolysis (One-way ANOVA followed by Bonferroni post
hoc test) |
EGCG at the concentrations of 1, 5 and 10 μM significantly stimulated
basal adipocyte lipolysis in the NPD group with the FFA concentrations of 453.67±25.57,
458.87±26.84 and 443.97±19.75 μM mL-1 PCV/ h,
respectively (p<0.05; n = 5) (Fig. 2).
When isoprenaline (0.1 μM) was added, the FFA concentration was significantly
increased to the level of 877.57±52.69 μM mL-1 PCV h-1
(p<0.05) (Fig. 1). The FFA level in the presence of isoprenaline
was calculated as 171.30±16.73% increase of that in the absence of isoprenaline
(basal lipolysis). EGCG at any of the concentrations tested (1, 5, 10 μM)
did not cause a significant change in isoprenaline-induced lipolysis in adipocytes
derived from the NPD-fed rats.
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Fig. 3: |
Effects of EGCG on isoprenaline-induced lipolysis in the NPD-group.
The results are expressed as the Mean±SEM (n = 5). There is no statistically
significant difference between groups. The statistical analysis was performed
by using One-way ANOVA followed by Bonferroni post hoc test. Adipocytes
were treated with 0.1 μM isoprenaline under the condition shown |
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Fig. 4: |
Effects of EGCG on basal adipocyte lipolysis in the HFD-group.
The results are expressed as the Mean±SEM (n = 4). *p<0.05 when
compared with basal lipolysis (One-way ANOVA followed by Bonferroni post
hoc test) |
In the condition of isoprenaline-induced lipolysis, the FFA concentrations
in the presence of EGCG at the concentrations of 1, 5 and 10 μM were 929.50±180.09,
936.43±76.63 and 831.85±58.38 μM mL-1 PCV h-1,
respectively (n = 5, Fig. 3).
Lipolytic effects of EGCG in adipocytes derived from the HFD-fed rats (HFD-group):
The FFA concentration in the basal lipolysis of adipocytes derived from the
HFD-fed rats was 407.49±70.42 μM mL-1 PCV h-1.
This was not statistical dissimilar to the FFA concentration found in the basal
lipolysis of adipocytes derived from the NPD-fed rats. EGCG at the concentration
of 5 μM significantly increased the basal lipolysis in adipocytes derived
from the HFD group with the FFA concentration of 1,091.75±220.56 μM
mL-1 PCV h-1 (p<0.05; n = 4, Fig. 4).
The basal adipocyte lipolysis was not significantly affected by the addition
of EGCG at the other concentrations tested (1 and 10 μM).
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Fig. 5: |
Effects of EGCG on isoprenaline-induced lipolysis in the HFD-group.
The results are expressed as the Mean±SEM (n = 5). There is no statistically
significant difference between groups. The statistical analysis was performed
by using One-way ANOVA followed by Bonferroni post hoc test. Adipocytes
were treated with 0.1 μM isoprenaline under the condition shown |
The FFA levels in the presence of EGCG at the concentrations of 1 and 10 μM
were modestly increased to the concentrations of 514.28±9.11 and 706.48±107.89
μM mL-1 PCV h-1, respectively (n = 4). However, these
levels did not reach a statistical significance.
Isoprenaline at the concentration of 0.1 μM significantly increased adipocyte
lipolysis in adipocytes derived from the HFD group with the FFA concentration
of 980.00±38.57 μM mL-1 PCV h-1 (p<0.05)
(Fig. 1). In the presence of isoprenaline, the FFA concentration
was increased by 140.51±9.46% of the basal lipolysis. EGCG at the concentrations
of 1 and 10 μM caused an increase in isoprenaline-induced lipolysis, with
the FFA concentrations of 1,356.16±262.97 and 1,699.70±110.94
μM mL-1 PCV h-1, respectively (n = 5). However, these
FFA concentrations were not statistically different from that in the presence
of isoprenaline alone. EGCG at the concentration of 5 μM did not cause
a significant change in the isoprenaline-induced lipolysis, with the FFA concentration
of 885.87±151.36 μM mL-1 PCV h-1 (n = 5, Fig.
5).
DISCUSSION
The body weight of the rats fed with HFD was not different from that of the
rats fed with NPD. This is similar to the results of Harris
(1991) and Collin et al. (2006) as well as
our previous finding (Pulbutr et al., 2011).
However, the weight of epididymal fat pads in the HFD-fed rats was significantly
higher than that in the NPD-fed rats. The similar findings were reported by
Naim et al. (1985) and Collin
et al. (2006). From their studies, after feeding with high fat diet
for 3 weeks, there was a significant increase in the weights of epididymal and
visceral fat pads.
From this study, EGCG at every concentration tested (1, 5 and 10 μM) significantly
stimulated basal adipocyte lipolysis in adipocytes isolated from the NPD-fed
rats. This is in accordance with the results from the study of Lee
et al. (2009a) which showed that 10 μM EGCG significantly increased
basal adipocyte lipolysis. However, from their study the lipolytic stimulating
action of EGCG was not detected when the lower concentration of 1 μM was
used. Our experiments were performed by using primary rat adipocytes whilst
3T3-L1 adipocytes were used in the study of Lee et al.
(2009a). The difference in adipocyte cell type may be the reason for the
discrepancy in the lipolytic response to EGCG found between the studies. In
addition, the lipolytic action of EGCG at the lower concentration (2.79 μM)
was also demonstrated recently in primary rat adipocytes by Ogasawara
et al. (2011).
The mRNA levels of lipolytic genes, including Hormone Sensitive Lipase (HSL)
enzyme and Adipose Triglyceride Lipase (ATGL) enzyme were found to be increased
in mice after feeding with high fat-diet supplemented with EGCG (0.2 or 0.5%
w/w) for 8 weeks (Lee et al. 2009b). Additionally,
it was shown from the same study that the mRNA levels of various adipogenic
genes, such as PPAR-γ, CCAAT Enhancer-binding Protein-α (C/EBP-α),
Sterol Regulatory Element-binding Protein-1c (SREBP-1c), adipocyte fatty acid-binding
protein (aP2), Lipoprotein Lipase (LPL) and Fatty Acid Synthase (FAS), were
also decreased in the mice fed with EGCG-supplemented high fat diet. Lee
et al. (2009a) revealed that when treated with 10 μM EGCG for
24 h, the mRNA level of HSL was dramatically increased in 3T3-L1 adipocytes.
The investigators thus concluded that EGCG increased adipocyte lipolysis via
induction of HSL mRNA expression. However, in our study, the lipolytic stimulating
action was demonstrated even when the adipocytes were treated with EGCG only
for 1 h. It remains unanswered whether the lipolytic stimulating action of EGCG
found here is also related to the changes in HSL mRNA expression.
It was reported recently that the lipolytic stimulating effect of EGCG was
abolished when the adipocytes were pre-incubated with MAPK/ERK kinase 1/2 (MEK1/2)
inhibitor (PD98059) (Ogasawara et al., 2011).
From their study, the levels of ERK1/2 phosphorylation and MEK1/2 phosphorylation
were also increased by EGCG treatment. These indicate that EGCG exerts its lipolytic
action via the activation of ERK1/2 pathway which is another essential pathway
for adipocyte lipolysis. Phosphorylation of HSL at Ser600 by ERK increases the
activity of HSL and consequently stimulates adipocyte lipolysis (Greenberg
et al., 2001).
EGCG did not produce its lipolytic stimulating action in adipocytes derived
from the NPD-fed rats in the condition of isoprenaline-induced lipolysis. Isoprenaline
was found to induce adipocyte lipolysis via both cAMP-dependent pathway and
ERK1/2 pathway (Greenberg et al., 2001). It was
reported that the lipolytic action of isoprenaline was depleted by approximately
30% when MEK inhibitors (PD98059 or U0126) were added simultaneously. It is
possible that isoprenaline and EGCG may stimulate adipocyte lipolysis by using
the similar ERK1/2 pathway. Thus, the lipolytic action of EGCG could not be
observed in the presence of isoprenaline. Present results also imply that EGCG
may not potentiate adipocyte lipolysis in the situations of sympathetic nervous
system stimulation such as physical exercise and physical or psychological stress.
However, EGCG also possesses other positive effects on lipid metabolism, such
as inhibition of adipogenesis, inhibition of lipid accumulation and stimulation
of lipid oxidation (Auvichayapat et al., 2008;
Chan et al., 2011). These beneficial effects
of EGCG may still exert during the sympathetic stimulation and the body weight
controlling action of EGCG thus may still be observed.
Adipocytes derived from the HFD-fed rats had a lower response to EGCG in the
condition of basal lipolysis. EGCG at every concentration tested (1, 5, 10 μM)
produced a significant lipolytic action in adipocytes derived from the NPD-fed
rats, but EGCG only at the concentration of 5 μM exhibited this action
in adipocytes derived from the HFD-fed rats. This may be due to the difference
in ERK pathway between adipocytes derived from the different diet type-fed rats.
ERK phosphorylation was found to be increased in mice fed with high fat diet
for 4, 6, 8 and 15 weeks (Ito et al., 2007).
ERK phosphorylation and activation of MAPK pathway has been found to play an
important role in adipocyte proliferation and differentiation. Bost
et al. (2005) showed that mice lacking ERK1 (ERK1-/-mice) were resistant
to diet-induced obesity and also protected from insulin resistance. The increased
level of phosphorylated ERK in adipocytes derived from HFD-fed rodents is likely
to be essential for adipocyte proliferation and differentiation. Most of the
increased level of phosphorylated ERK may be shifted to the adipocyte proliferation
and differentiation pathways, thus less amount of phosphorylated ERK would be
available for the activation of ERK-related lipolytic pathway which involves
in the lipolytic action of EGCG. This may partly be the reason why adipocytes
derived from the HFD-fed rats had the lower basal lipolytic response to EGCG.
Although ERK1/2 is activated early in the differentiation process, deactivation
of ERK1/2 is needed during adipogenesis to enhance terminal differentiation
(Gehart et al., 2010). According to this, it
can be alternatively proposed that ERK pathway may be less activated in adipocytes
derived from the HFD-fed rats, thus the lipolytic stimulating action of EGCG
was lessened. However, further study is needed to prove these speculations.
It is interesting that in adipocytes derived from the HFD-fed rats, EGCG at
the concentration of 10 μM slightly increased basal lipolysis, but the
level did not reach a significant difference. Further experiment thus should
be performed with more various concentrations of EGCG to investigate whether
EGCG performs its lipolytic-stimulating action in a concentration-dependent
manner in HFD-derived adipocytes.
From this study, EGCG did not produce a significant lipolytic stimulating action
in the presence of isoprenaline in adipocytes derived from both the NPD-fed
rats and the HFD-fed rats. However, EGCG at the highest concentration tested
(10 μM) tended to produce a lipolytic stimulating effect in adipocytes
derived from the HFD-fed rats, although its lipolytic stimulating action did
not reach a statistical significance. The reason for the increase in lipolytic
response to EGCG in the presence of isoprenaline in the HFD-fed rat derived
adipocytes is still unknown. It is not known if there is an alteration in isoprenaline-induced
lipolytic pathway in HFD-derived adipocytes. In adipocytes derived from the
HFD-fed rats, isoprenaline may probably act mainly via ERK-independent lipolytic
pathway. The ERK-dependent lipolytic pathway is thus reserved for EGCG activation.
Thus, the lipolytic stimulating action of EGCG can be observed more clearly.
It has been documented that HFD feeding affects on various key components involving
in adipocyte lipolysis such as perilipin, HSL enzyme, ATGL enzyme (Collin
et al., 2006; Gaidhu et al., 2010).
The modifications of these proteins may partly be the reason for the dissimilar
responses to EGCG in adipocytes derived from the different diet type-fed rats.
In conclusion, EGCG at every concentration tested (1, 5 and 10 μM) significantly
stimulated basal adipocyte lipolysis in the NPD-fed rat derived adipocytes but
a significant lipolytic stimulating action of EGCG was found only when 5 μM
EGCG was added in adipocytes derived from the HFD-fed rats. Thus, adipocytes
derived from the HFD-fed rats were less responsive to the lipolytic action of
EGCG in the condition of basal lipolysis. Present findings partially explain
and confirm the mechanism of weight-controlling action of EGCG. In addition,
the results found here also imply that EGCG possesses the protective role against
obesity since its lipolytic action was prominent only when over accumulation
of the adipose tissue has not been found yet. EGCG was likely to produce less
lipolytic stimulating action in the condition of isoprenaline-induced lipolysis
in adipocytes derived from both the NPD-fed rats and the HFD-fed rats. Although
the reason for the difference in EGCG response found in this study can be reasonably
proposed as mentioned earlier, further study is essentially required to prove
those speculations, especially in the molecular aspects.
ACKNOWLEDGMENTS
This study was financially supported by Mahasarakham University research grant
year 2012. We thank the Faculty of Pharmacy, Mahasarakham University for the
laboratory support. We would like to express our gratitude to Associate Professor
Songsak Jumpawadee, Faculty of Veterinary Medicine and Animal Sciences, Mahasarakham
University for preparation of animal diet. We are also grateful to Dr. Benjamart
Cushnie and Dr. Sakulrat Rattanakiat for their useful comments on the project.
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