Antihyperlipidemic and antioxidant activities of the ethanolic extract of Garcinia cambogia on high fat diet-fed rats

Ramalingam Sripradha 1 , Magadi Gopalakrishna Sridhar 1 , and Nachimuthu Maithilikarpagaselvi 1
  • 1 Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Ramalingam Sripradha, Magadi Gopalakrishna Sridhar and Nachimuthu Maithilikarpagaselvi

Abstract

Background: The study investigated the antihyperlipidemic and antioxidant activities of the ethanolic extract of Garcinia cambogia on high fat diet-fed rats.

Methods: The phytochemical constituents, total polyphenol content and ferric reducing antioxidant power (FRAP) were estimated in the G. cambogia extract (GE). Male Wistar rats were fed with either standard rodent diet or 30% high-fat diet and administered with GE at a dose of 400 mg/kg body weight/day for 10 weeks. At the end, lipid profile and oxidative stress parameters were estimated.

Results: The analyses revealed the presence of carbohydrates, proteins, sterols, tannins, flavonoids and saponins in GE. The total polyphenol content and FRAP of GE were 82.82±7.64 mg of gallic acid equivalents and 260.49±10.18 µM FRAP per gram of the GE. High-fat feeding elevated plasma total cholesterol (TC), triacylglycerol (TAG), non-high-density lipoprotein-cholesterol (non-HDL-C), malondialdehyde (MDA), reduced HDL-C and blood antioxidants, glutathione (GSH), glutathione peroxidase (GPx), catalase. Increase in total oxidant status (TOS), oxidative stress index (OSI) and decrease in the total antioxidant status (TAS) were observed in plasma, liver and kidney of fat-fed rats. Administration of GE decreased food intake, plasma TC, TAG, non HDL-C, MDA, increased HDL-C and blood antioxidants GSH, GPx, catalase. GE also reduced TOS, OSI and elevated TAS in plasma and liver of fat-fed rats. Renal OSI was significantly reduced upon GE treatment.

Conclusions: Our study demonstrated that GE is effective in ameliorating high-fat-diet-induced hyperlipidemia and oxidative stress.

Introduction

Obesity, a global health problem, occurs due to the imbalance in energy intake and expenditure resulting in accumulation of excess body fat [1]. As per the World Health Organization (WHO) estimate in 2014, more than 1.9 billion adults, 18 years and older, were overweight; of these over 600 million people were obese [2]. Obesity is associated with several metabolic complications such as hyperlipidemia, hypertension, diabetes mellitus and cardiovascular diseases [3]. In addition to genetic predisposition, consumption of foods rich in fat contributes to the development of obesity and its associated comorbidities [4]. Ingestion of fat-rich diet for a long period leads to dyslipidemia and steatosis [5]. Disorder of lipoprotein metabolism is defined as dyslipidemia which is characterized by increased plasma levels of total cholesterol (TC), triacylglycerol (TAG), low-density lipoprotein-cholesterol (LDL-C) with decreased high-density lipoprotein-cholesterol (HDL-C) levels. Dyslipidemia contributes to several cerebrovascular and cardiovascular complications such as stroke, atherosclerosis and hypertension [6, 7].

It has been reported that diet-induced obesity triggers deposition of excess fat in adipose as well as nonadipose target tissues such as liver and kidney causing excessive generation of highly reactive molecular species (ROS) leading to oxidative damage [8, 9]. Inadequate neutralization of the oxidants by the antioxidants such as superoxide dismutase (SOD), catalase, glutathione S-transferase (GST) and glutathione peroxidase (GPx) further aggravates the free radical-mediated damage. Persistent imbalance between the production of highly reactive free radicals and antioxidant defenses results in oxidative stress [10]. Oxidants generated due to oxidative stress trigger the activation of several phosphorylation cascades and leads to the stimulation of mitogen-activated protein kinases (MAPKs) and nuclear factor κB (NF-κB) [11]. In the absence of an appropriate compensating antioxidant network, the system becomes overwhelmed, leading to the activation of stress-sensitive signaling pathways which causes generation of several gene products, resulting in damage to cellular components like nucleic acids, lipids and proteins [12]. Hence it is imperative to prevent the detrimental physiological alterations induced by oxidative stress.

Consumption of diets enriched with antioxidants or plant products having vital phytochemicals may provide beneficial effects in alleviating these stress-mediated complications with minimal adverse effects than currently available pharmacotherapeutic strategies [13]. Garcinia cambogia also called Malabar tamarind belongs to the family Guttiferae and is grown in Southeast Asia. The fruit has a characteristic sweet and sour taste, commonly used as food preservative, carminative and flavoring agent [14]. The extract of G. cambogia is used in Indian medicine for the treatment of ulcers, hemorrhoids, diarrhea, dysentery and certain types of cancer [15]. The fruit rind has been reported to contain organic acids like (–) Hydroxycitric acid (HCA), citric acid, malic acid, xanthones, flavonoids, benzophenones like garcinol/camboginol and isoxanthohumol [16]. Animal experiments have reported anti-inflammatory and antiulcerogenic properties of G. cambogia extract (GE) [17, 18]. To the best of our knowledge there are no previous reports stating the beneficial effects of G. cambogia on oxidative stress associated with diet-induced obesity. Hence the present study was designed to investigate the beneficial effects of GE against dyslipidemia and oxidative stress in high-fat-fed rats.

Figure 1:
Figure 1:

Effect of Garcinia cambogia extract on high-fat-diet-induced dyslipidemia and oxidative stress.

Citation: Journal of Complementary and Integrative Medicine 13, 1; 10.1515/jcim-2015-0020

The figure represents the graphical summary of the effect of G. cambogia extract (GE) on high-fat-diet-induced dyslipidemia and oxidative stress in male Wistar rats. Pink colored arrow indicates the inhibitory effect of G. cambogia extract. TC, total cholesterol; TAG, triacylglycerol; non-HDL-C, non-high-density lipoprotein-cholesterol; HDL-C, high-density lipoprotein-cholesterol; MDA, malondialdehyde; TOS, total oxidant status; OSI, oxidative stress index; TAS, total antioxidant status; GSH, glutathione; GPx, glutathione peroxidase.

Materials and methods

Animals

Five-month-old male albino Wistar rats (n=40) were obtained from the Institute Central Animal House, JIPMER. The animals were housed in polycarbonate cages (2 rats/cage) and maintained at 25±1  °C with a 12 h light/12 h dark cycle. The animals had free access to food and water provided ad libitum. The study was approved by the Institute Scientific Advisory Committee and conducted in the Department of Biochemistry, JIPMER. Animal handling and experimental procedures were approved by the Institutional Animal Ethics Committee.

Preparation of ethanolic extract of G. cambogia

Fresh fruits of G. cambogia were obtained from Kerala, India. The fruit was identified and authenticated by the French Institute of Pondicherry, Puducherry, India (Accession No. 25821 dated Jan 10, 2012). G. cambogia fruit extract was prepared based on the extraction procedure of Oluyemi et al. with modifications [19]. The fruits were washed and seeds were removed. The fruit rinds were sun dried, ground and crudely extracted with 70% v/v ethanol by shaking for 24 h at room temperature. The solution was filtered and the filtrate was evaporated under reduced pressure to obtain a semisolid residue. The residual material was stored at 4  °C until use.

Experimental protocol

After 1 week of adaptation, the animals were randomly divided into four groups with ten rats in each.

  • Group 1: Control, rats received standard rodent diet.
  • Group 2: Control+GE, rats received standard rodent diet and GE.
  • Group 3: High-fat diet, rats received 30% high-fat diet.
  • Group 4: High-fat diet+GE, rats received 30% high-fat diet and GE.

The control rats were fed with standard rodent diet and the total energy of the standard rodent diet was 3.2 kcal/g. The purified high-fat diet mixture was prepared according to Hsu et al. [20], with 30.35% of total calories derived from carbohydrate, 21.8% from protein and 53.78% from fat. The total energy of the high-fat diet mixture was found to be 5.02 kcal/g. The composition of high-fat diet and control diet is given in Table 1. Pilot studies were conducted with various concentrations of GE and 400 mg/kg body weight was chosen as the effective dose. The GE was dissolved in drinking water and a dose of 400 mg/kg body weight [19] of the GE was administered to each rat in groups 2 and 4 through oral gavage every day throughout the experimental period. The rats in the different groups received their respective diets and GE for an experimental duration of ten weeks.

At the end of the experiment, fasting blood samples were collected from all rats via tail vein. The blood samples were then centrifuged at 3,500 rpm for 10 min, the plasma was separated and stored at –80  °C till analysis. The animals were sacrificed, tissues like liver and kidney were frozen immediately in liquid N2 and kept at –80  °C for further analysis. The chemicals used for all assays were of analytical grade, obtained from Merck (India) and SRL (India).

Table 1:

Composition of high-fat diet and control diet.

High-fat diet ingredients(g/100 g)
Casein26.0
Corn starch16.0
Sucrose16.0
Cellulose6.1
Safflower oil1.0
Butter29.0
AIN-76 vitamin mixture1.2
AIN-76 mineral mixture4.2
Choline0.2
DL-methionine0.3

AIN-76 Vitamin mixture (perkg mixture): Thiamin.HCl 600 mg, riboflavin 600 mg, pyridoxine.HCl 700 mg, nicotinic acid 3 g, D-calcium pantothenate 1.6 g, folic acid 200 mg, D-biotin 20 mg, cyanocobalamin (vitamin B-12) 1 mg, retinyl palmitate or acetate (vitamin A) stabilized powder to provide 400,000 IU vitamin A activity or 120,000 retinol equivalents, DL-α-tocopheryl acetate (vitamin E) stabilized powder to provide 5,000 IU vitamin E activity, cholecalciferol (vitamin D3) 2.5 mg (100,000 IU), menaquinone (vitamin K) 5.0 mg, sucrose finely powdered to make 1,000 g. AIN-76 Mineral mixture (g/kg mixture): Calcium phosphate, dibasic (CaHPO4) 500.0, sodium chloride (NaCl) 74.0, potassium citrate monohydrate (K3C6H5O7.H2O) 220.0, potassium sulfate (K2SO4) 52.0, magnesium oxide (MgO) 24.0, manganous carbonate (43–48% Mn) 3.5, ferric citrate (16–17% Fe) 6.0, zinc carbonate (70% ZnO) 1.6, cupric carbonate (53–55% Cu) 0.3, potassium iodate (KIO3) 0.01, sodium selenite (Na2SeO3.5H2O) 0.01, chromium potassium sulfate [CrK(SO4)2.12H2O] 0.55, sucrose, finely powdered to make 1,000 g. The total energy of the high-fat diet was 5.02 kcal/g. Composition of the control diet: 60% (w/w) starch, 22.08% (w/w) protein, 4.38% (w/w) fat and the total energy of the control diet was 3.2 kcal/g.

Estimation of parameters

  1. (i)Analysis of phytochemical constituents, total polyphenol and ferric reducing antioxidant power (FRAP) of the GE

GE was dissolved at a concentration of 1 mg/mL in dimethyl sulfoxide (DMSO) [21] and used for all the in vitro analysis performed. The phytochemical constituents such as carbohydrates, proteins, sterols, tannins, flavonoids and saponins were analyzed qualitatively using standard procedures [22].

  1. (ii)Determination of total polyphenol content

The amount of total polyphenols in the GE was estimated using Folin–Ciocalteu reagent by the method of Singleton and Rossi and Velioglu et al. [23, 24]; 0.1 mL of the GE solution (1 mg/mL) was mixed with 0.75 mL of Folin–Ciocalteu reagent (1: 10 diluted with distilled water). The mixture was allowed to stand for 5 min at 22  °C. To this 0.75 mL of 6% sodium carbonate is added, mixed and incubated for 90 min at 22  °C in the dark. The absorbance of the samples was read at 725 nm using UV/visible spectrophotometer. Results were obtained from a standard graph of gallic acid (0–0.1 mg/mL) and expressed as mg of gallic acid equivalents (GAE)/g of the GE. The assay was repeated thrice under the same conditions for three consecutive days and the mean value was obtained.

  1. (iii)Determination of reducing ability by FRAP assay

FRAP assay of GE was assessed by the method of Benzie et al. [25]: 300 µl of the FRAP reagent (acetate buffer, 2,4,6-tripyridyl-s-triazine (TPTZ) and FeCl3) was mixed with 10 µL of the GE solution (1 mg/mL) and incubated at room temperature for 4 min. The absorbance was read at 593 nm using UV/visible spectrophotometer. Results were obtained from a standard graph of FeSO4 (0–1000 µmol/L) and expressed as µM FRAP/g of the GE. The assay was repeated thrice under the same conditions for three consecutive days and the mean value was obtained.

  1. (iv)Estimation of lipid profile and oxidative stress parameters

Specific reagent kits were used for the estimation of plasma TC (Genuine Biosystems, Chennai, India), TAG (Agappe Diagnostics, Kerala, India), HDL-C (Lab-care Diagnostics, India) and these kits were adapted to automated clinical chemistry analyzer (AU-400, Olympus, UK) for further analyses. The non-HDL-C was calculated by subtracting TC and HDL-C. The whole blood reduced glutathione (GSH) content was measured by the method of Beutler et al. [26]. The activities of the erythrocyte antioxidant enzymes GPx and catalase were estimated by Wendel et al. [27] and Aebi et al. [28], respectively. Plasma malondialdehyde (MDA) level was measured by high-performance liquid chromatography by the method of Rajiv Agarwal et al. [29]. Liver and kidney tissues were homogenized with 0.1 M ice cold Tris–HCl buffer (pH 7.4, 10% w/v) [30]. The homogenates were centrifuged at 14,000 × g for 15 min at 4  °C and the supernatants were used for the estimation of total oxidant status (TOS) and total antioxidant status (TAS). The protein concentration in the liver and kidney homogenates was determined by the method of Lowry et al. [31]. TOS in plasma and tissue samples was estimated by the method of Ozcan Erel [32]. TAS in plasma and tissue samples was measured by the ferric reducing ability of plasma based on the method of Benzie et al. [25]. Oxidative stress index (OSI) was calculated by the formula (TOS/TAS)×100.

Statistical analysis

The results were represented as mean±SD. Differences between the groups were analyzed by one-way analysis of variance (ANOVA) with Tukey as post hoc test using Statistical Package of Social Service (SPSS version 19). A p-Value<0.05 was considered as statistically significant.

Results

  1. (i)Phytochemical screening, total polyphenol content and FRAP of GE (Tables 2 and 3).

Phytochemical screening of the GE showed the presence of carbohydrates, proteins, sterols, tannins, flavonoids and saponins. The total polyphenol content was found to be 82.82±7.64 mg GAE/g of the GE. FRAP of GE was found to be 260.49±10.18 µmol/L FRAP/g of the GE.

  1. (ii)Effect of GE on food intake, plasma lipid profile in control and high-fat-fed rats (Table 4).

Table 2:

Phytochemical analyses of the Garcinia cambogia extract (GE).

Sl. NoPhytochemical compoundsResults
1Carbohydrates+
2Proteins+
3Sterols+
4Tannins+
5Flavonoids+
6Saponins+

+Present.

Table 3:

Total polyphenol content and ferric reducing antioxidant power (FRAP) of the Garcinia cambogia extract (GE).

Concentration of the GETotal polyphenol contentaFerric reducing antioxidant powerb
1 mg/mL82.82±7.64260.49±10.18

Data were represented as mean±SD (n=3). aExpressed as mg gallic acid equivalents/g of the GE and bexpressed as µM FRAP/g of the GE.

Table 4:

Effect of Garcinia cambogia extract (GE) on food intake, plasma lipid profile in control and high-fat-fed rats.

Sl. NoParametersControlControl+GEHFDHFD+GE
1Food intake (g/day)14.92±1.0914.03±1.0615.82±1.1114.48±0.69b
2Total cholesterol (mg/dL)49.30±4.2447.10±4.8270.10±9.88a59.40±7.62b
3Triacylglycerol (mg/dL)78.00±9.7177.30±11.10135.20±16.31a110.50±14.14b
4HDL-C (mg/dL)30.00±3.0231.70±2.8319.70±3.13a24.40±2.67b
5Non-HDL-C (mg/dL)19.30±4.9715.40±4.8650.40±10.36a35.00±9.20b

Data were represented as mean±SD (n=10). aSignificant as compared with control rats (p<0.05). bSignificant as compared with HFD rats (p<0.05). HFD, high-fat diet; GE, Garcinia cambogia extract; HDL-C, high-density lipoprotein-cholesterol.

The average food intake per day for each group (10 rats) throughout the entire experimental duration of ten weeks is represented in Table 4. There was no significant change in the food intake between control and high-fat-fed rats. Supplementation of GE decreased food intake in rats fed with high-fat diet. High-fat feeding significantly elevated plasma TC, TAG, non HDL-C and reduced HDL-C levels when compared to control rats. Administration of GE along with high-fat diet significantly reduced plasma TC, TAG, non HDL-C and increased HDL-C levels.

  1. (iii)Effect of GE on oxidative stress parameters in control and high-fat-fed rats (Tables 58).

Table 5:

Effect of Garcinia cambogia extract (GE) on blood antioxidant enzymes in control and high-fat-fed rats.

Sl. NoParametersControlControl+GEHFDHFD+GE
1GSH (mg/gHb)4.08±0.514.10±0.482.30±0.42a2.88±0.43b
2GPx (U/gHb)78.36±8.3580.35±5.1043.74±6.41a56.32±7.36b
3Catalase (K/mL)71.69±6.9174.21±5.1740.64±7.24a51.04±7.91b

Data were represented as mean±SD (n=10). aSignificant as compared with control rats (p<0.05). bSignificant as compared with HFD rats (p<0.05). HFD, high-fat diet; GE, Garcinia cambogia extract; GSH, glutathione; GPx, glutathione peroxidase.

Table 6:

Effect of Garcinia cambogia extract (GE) on plasma oxidative stress parameters in control and high-fat-fed rats.

Sl. NoParametersControlControl+GEHFDHFD+GE
1MDA (μmol/L)1.84±0.491.79±0.414.83±0.71a3.77±0.67b
2TOS (µmol H2O2 equiv/L)13.11±2.1412.16±2.4829.10±4.19a21.01±3.05b
3TAS (μmol/L)545.25±53.46549.29±65.13338.39±56.45a426.32±60.74b
4OSI2.42±0.462.26±0.648.92±2.43a5 ±0.94b

Data were represented as mean±SD (n=10). aSignificant as compared with control rats (p<0.05). bSignificant as compared with HFD rats (p<0.05). HFD, high-fat diet; GE, Garcinia cambogia extract; MDA, malondialdehyde; TOS, total oxidant status; TAS, total antioxidant status; OSI, oxidative stress index.

Table 7:

Effect of Garcinia cambogia extract (GE) on hepatic oxidative stress parameters in control and high-fat-fed rats.

Sl. NoParametersControlControl+GEHFDHFD+GE
1TOS (μmol H2O2 equiv/mg of protein)2.42±0.472.36±0.553.73±0.62a2.98±0.46b
2TAS (μmol/mg of protein)70.35±7.1171.27±6.4246.88±5.64a57.68±6.02b
3OSI3.47±0.743.33±0.758.07±1.72a5.21±0.90b

Data were represented as mean±SD (n=10). aSignificant as compared with control rats (p<0.05). bSignificant as compared with HFD rats (p<0.05). HFD, high-fat diet; TOS, total oxidant status; TAS, total antioxidant status; OSI, oxidative stress index.

Table 8:

Effect of Garcinia cambogia extract (GE) on renal oxidative stress parameters in control and high-fat-fed rats.

Sl. NoParametersControlControl+GEHFDHFD+GE
1TOS (μmol H2O2equiv/mg of protein)2.11±0.532.06±0.442.91±0.44a2.43±0.31
2TAS (μmol/mg of protein)60.77±8.0261.89±6.6949.71±8.38a56.08±7.39
3OSI3.45±0.743.40±1.016.02±1.41a4.38±0.71b

Data were represented as mean±SD (n=10). aSignificant as compared with control rats (p<0.05). bSignificant as compared with HFD rats (p<0.05). HFD, high-fat diet; GE, Garcinia cambogia extract; TOS, total oxidant status; TAS, total antioxidant status; OSI, oxidative stress index.

Rats fed with fat-rich diet showed significant increase in the plasma MDA, decrease in the GSH content and activities of the antioxidant enzymes GPx and catalase when compared to control rats. There was elevation in the levels of TOS, OSI and reduction in the TAS of plasma, liver and kidney of high-fat-fed rats. Treatment with GE significantly increased the blood antioxidants – GSH content and activities of GPx and catalase. There was also decrease in the plasma MDA levels upon GE supplementation. GE also reduced TOS, OSI and elevated TAS in plasma and liver of rats fed with fat-rich diet. Reduction in the renal OSI was observed with administration of GE along with high-fat diet.

Discussion

The emerging problem of obesity causes disability, reduces productivity, shortens life span and increases the risk of comorbidities such as diabetes, hypertension, cardiovascular diseases and certain types of cancer [33]. In addition to genetic influence, environmental factors such as Western diet increase the risk of obesity in developing countries [4]. The clamor for alternative strategies with minimal adverse effects has led to the search of newer drugs for the management of obesity. G. cambogia is a plant used in Indian medicine for various ailments [15]. In our study we investigated the beneficial effects of G. cambogia against high-fat-induced dyslipidemia and redox imbalance.

In our study, no significant change was observed in the food intake between control and high-fat-fed rats. Treatment with GE reduced the food intake in fat-fed rats. The observed reduction in the food intake due to GE administration could be due to the vital phytochemicals present in it. We also found rats fed with high-fat diet showed increased body weight compared to control rats and administration of GE significantly reduced the body weight in high-fat-fed rats [34]. High-fat feeding resulted in dyslipidemic changes as illustrated by elevated plasma levels of TC, TAG, non HDL-C and reduced HDL-C when compared to control rats. Our findings were in agreement with Jang et al. 2013 who have reported similar effects on high-fat intake [35]. The non-HDL-C fraction comprises of apolipoprotein B containing lipoproteins such as very low density lipoprotein-cholesterol (VLDL-C), intermediate density lipoprotein-cholesterol (IDL-C), LDL-C, chylomicron remnants and lipoprotein a. Non-HDL-C is an accepted index of apo B in clinical practice and is considered as a marker of cardiovascular disease [36]. There is evidence that dyslipidemia is positively associated with various metabolic and vascular complications [6, 7]. We found that administration of GE along with high-fat diet significantly reduced plasma levels of TC, TAG, non HDL-C and elevated HDL-C. The cumulative effect of various organic acids like (–)HCA, citric acid, malic acid, secondary metabolites such as xanthones, flavonoids, benzophenones like garcinol/camboginol and isoxanthohumol present in the fruit rind of G. cambogia is responsible for the observed hypolipidemic effects [16]. Among the organic acids, HCA is a competitive inhibitor of the citrate cleavage enzyme, ATP-citrate lyase and this inhibitory effect leads to reduced rate of lipogenesis resulting in hypolipidemic effects [37]. Flavonoids, xanthones and benzophenones are metabolites having antioxidant properties [38]. It has been shown that administration of flavonoids isolated from G. cambogia fruit reduced lipid levels in rats fed with cholesterol-rich diet by decreasing lipogenesis and enhancing degradation of lipids [39]. Oluyemi et al. have reported that the seeds of G. cambogia also show erythropoietic and antiobesity effects in high-fat-fed rats [19]. In line with these findings we suggest that the vital phytochemicals in G. cambogia contribute for the antihyperlipidemic property and supplementation of GE may help in the amelioration of obesity-related metabolic and vascular complications.

We found rats fed with high-fat diet showed elevated plasma MDA levels in association with reduced activities of blood antioxidant enzymes – GSH, GPx, and catalase. There were also increased levels of TOS, OSI and reduced TAS in plasma, liver and kidney of fat-fed rats. In obesity, altered lipid homeostasis leads to excess fat accumulation in adipose and nonadipose tissues like liver, kidney and causes cellular damage. This in turn elevates the production of cytokines which creates local inflammation and generates ROS [40]. Imbalance between the production of ROS and the antioxidant defense leads to oxidative stress and associated damage [10]. The body has an effective defense mechanism consisting of endogenous antioxidants such as GST, SOD, glutathione reductase (GRD), catalase, GPx and GSH to offer protection against these free radical mediated damage. Overproduction of ROS causes damage to biomolecules like proteins, lipids and DNA and leads to cellular damage [41]. Lipid peroxidation by ROS leads to the generation of highly toxic by-product MDA [42]. This causes damage by diffusing to more distant cellular targets from their origin since they have longer half-life than ROS [43].

Administration of GE along with high-fat diet decreased plasma and hepatic TOS and OSI. There was significant decrease in the renal OSI and plasma MDA levels upon treatment with GE. GE supplementation also showed increase in the blood antioxidants – GSH, GPx, catalase, plasma and hepatic TAS. The phytochemical analyses of GE showed the presence of carbohydrates, proteins, sterols, saponins, tannins and flavonoids. Saponins and tannins have been reported to have anti-inflammatory effect [44, 45]. Flavonoids are a group of polyphenols, having antioxidant and anti-inflammatory activities [46]. Furthermore the total polyphenol content of the GE was found to be 82.82±7.64 mg GAE/g of the GE. Phenolic compounds are a large group of naturally occurring secondary plant metabolites, possessing antiapoptotic, anti-inflammatory, antioxidant, antiaging and anticancer properties [47]. The Ferric Reducing Antioxidant Power of the GE was found to be 260.49±10.18 µM FRAP/g of the GE. Thus it is evident that the antioxidants present in the GE contribute for the improvement of the redox imbalance. From our study we found hyperlipidemia and oxidative stress play critical role in the pathogenesis of various complications in diet-induced obesity. The antioxidants present in the GE contribute to the prevention of these metabolic derangements (Figure 1) and this suggests the use of G. cambogia as a therapeutic strategy for relieving the stress-mediated complications in obesity.

Conclusions

The present study confirmed that excess intake of fat-rich diet leads to the development of obesity-associated complications like dyslipidemia and oxidative stress. We found that GE is effective in improving high-fat diet-induced dyslipidemia and redox imbalance. The various phytochemicals present in the GE account for the observed hypolipidemic and antioxidant effects. Thus we suggest G. cambogia fruit could be included as a dietary supplement which will mitigate these diet-induced complications.

Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

Research funding: None declared.

Employment or leadership: None declared.

Honorarium: None declared.

Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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  • 14. Saito M, Ueno M, Ogino S, Kubo K, Nagata J, Takeuchi M. High dose of Garcinia cambogia is effective in suppressing fat accumulation in developing male Zucker obese rats, but highly toxic to the testis. Food Chem Toxicol Int J Publ Br Ind Biol Res Assoc 2005;43:411–19.

    • Crossref
    • Export Citation
  • 15. Duke J, Bogenschutz-Godwin M, duCellier J, Duke PA. Handbook of medicinal herbs, 2nd ed. Boca Raton, FL: CRC Press, 2002:481.

  • 16. Chuah LO, Ho WY, Beh BK, Yeap SK. Updates on antiobesity effect of Garcinia Origin (-)-HCA. Evid Based Complement Altern Med ECAM 2013;doi: 10.1155/2013/751658.

  • 17. Dos Reis SB, de Oliveira CC, Acedo SC, Miranda DD, da C, Ribeiro ML, Pedrazzoli J, et al. Attenuation of colitis injury in rats using Garcinia cambogia extract. Phytother Res PTR 2009 Mar23:324–9.

    • Crossref
    • Export Citation
  • 18. Mahendran P, Vanisree AJ, Shyamala Devi CS. The antiulcer activity of Garcinia cambogia extract against indomethacin-induced gastric ulcer in rats. Phytother Res PTR 2002;16:80–3.

    • Crossref
    • Export Citation
  • 19. Oluyemi KA, Omotuyi IO, Jimoh OR, Adesanya OA, Saalu CL, Josiah SJ. Erythropoietic and anti-obesity effects of Garcinia cambogia (bitter kola) in Wistar rats. Biotechnol Appl Biochem 2007 Jan46:69–72.

    • Crossref
    • PubMed
    • Export Citation
  • 20. Hsu SC, Huang CJ. Reduced fat mass in rats fed a high oleic acid-rich safflower oil diet is associated with changes in expression of hepatic PPARalpha and adipose SREBP-1c-regulated genes. J Nutr 2006 Jul136:1779–85.

    • Crossref
    • PubMed
    • Export Citation
  • 21. Shivapriya S, Sandhiya S, Subhasree N, Aruna A, Dubey G. In vitro assessment of antibacterial and antioxidant activities of fruit rind extracts of Garcinia cambogia. L Int J Pharm Pharm Sci 2013;5:254–7.

  • 22. Harborne J. Phytochemical methods. New Delhi: Springer (India) Pvt. Ltd, 2005:17.

  • 23. Singleton VL, RossiJr JA. Colorimetry of total phenolics with phosphomolybdic-phosphotungstic acid reagents. AmJ Enol Vitic 1965;16:144–58.

  • 24. Velioglu YS, Mazza G, Gao L, Oomah BD, Activity A. Total phenolics in selected fruits, vegetables, and grain products. J Agric Food Chem 1998;46:4113–17.

    • Crossref
    • Export Citation
  • 25. Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: the FRAP assay. Anal Biochem 1996 Jul 15239:70–6.

    • Crossref
    • PubMed
    • Export Citation
  • 26. Beutler E, Duron O, Kelly BM. Improved method for the determination of blood glutathione. J Lab Clin Med 1963;61:882–8.

    • PubMed
    • Export Citation
  • 27. Wendel A. Glutathione peroxidase. Methods Enzymol 1981;77:325–33.

  • 28. Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121–6.

  • 29. Agarwal R, Chase SD. Rapid, fluorimetric-liquid chromatographic determination of malondialdehyde in biological samples. J Chromatogr B Analyt Technol Biomed Life Sci 2002;775:121–6.

    • Crossref
    • PubMed
    • Export Citation
  • 30. Sellamuthu PS, Arulselvan P, Kamalraj S, Fakurazi S, Kandasamy K. Protective nature of mangiferin on oxidative stress and antioxidant status in tissues of streptozotocin-induced diabetic rats. ISRN Pharmacology 2013;2013:750109 (10 pages).

    • PubMed
    • Export Citation
  • 31. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem 1951 Nov193:265–75.

    • PubMed
    • Export Citation
  • 32. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38:1103–11.

    • Crossref
    • PubMed
    • Export Citation
  • 33. Ahima RS. Digging deeper into obesity. J Clin Invest 2011;121:2076–9.

  • 34. Sripradha R, Magadi SG. Efficacy of garcinia cambogia on body weight, inflammation and glucose tolerance in high fat fed male wistar rats. J Clin Diagn Res JCDR. 2015 Feb;9(2):BF01–4.

    • Crossref
    • Export Citation
  • 35. Jang WS, Choung SY. Antiobesity effects of the ethanol extract of Laminaria japonica Areshoung in high-fat-diet-induced obese rat. Evid-Based Complement Altern Med ECAM 2013;2013:492807.

  • 36. Suchitra M, Kumar M, Bitla A, Rao A, Alok S. Atherogenic dyslipidemia in diabetic nephropathy: lipoprotein (a), lipid ratios and atherogenic index. Int J Res Med Sci 2013;1:455–9.

    • Crossref
    • Export Citation
  • 37. Sullivan AC, Triscari J, Hamilton JG, Miller ON, Wheatley VR. Effect of (-)-hydroxycitrate upon the accumulation of lipid in the rat. I Lipogenesis Lipids 1974;9:121–8.

  • 38. Tharachand IS. Mythili avadhani. Medicinal properties of Malabar Tamarind [Garcinia cambogia (Gaertn.) DESR. Int J Pharm Sci Rev Res 2013;19:101–7.

  • 39. Asha SK, Anila L, Vijayalakshmi NR. Flavonoids from Garcinia cambogia lower lipid levels in hypercholesterolemic rats. Food Chem 2001;72:289–94.

    • Crossref
    • Export Citation
  • 40. Peng Y, Rideout D, Rakita S, Lee J, Murr M. Diet-induced obesity associated with steatosis, oxidative stress, and inflammation in liver. Surg Obes Relat Dis Off J Am Soc Bariatr Surg 2012;8:73–81.

  • 41. Melov S. Mitochondrial oxidative stress. Physiologic consequences and potential for a role in aging. Ann N Y Acad Sci 2000;908:219–25.

    • PubMed
    • Export Citation
  • 42. Slatter DA, Bolton CH, Bailey AJ. The importance of lipid-derived malondialdehyde in diabetes mellitus. Diabetologia 2000;43:550–7.

    • Crossref
    • PubMed
    • Export Citation
  • 43. Meng R, Zhu D-L, Bi Y, Yang D-H, Wang Y-P. Anti-oxidative effect of apocynin on insulin resistance in high-fat diet mice. Ann Clin Lab Sci 2011;41:236–43.

    • PubMed
    • Export Citation
  • 44. Just MJ, Recio MC, Giner RM, Cuéllar MJ, Máñez S, Bilia AR, et al. Anti-inflammatory activity of unusual lupane saponins from Bupleurum fruticescens. Planta Med 1998;64:404–7.

    • Crossref
    • PubMed
    • Export Citation
  • 45. Ruch RJ, Cheng SJ, Klaunig JE. Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea. Carcinogenesis 1989;10:1003–8.

    • Crossref
    • PubMed
    • Export Citation
  • 46. Salah N, Miller NJ, Paganga G, Tijburg L, Bolwell GP, Rice-Evans C. Polyphenolic flavanols as scavengers of aqueous phase radicals and as chain-breaking antioxidants. Arch Biochem Biophys 1995;322:339–46.

    • Crossref
    • PubMed
    • Export Citation
  • 47. Han X, Shen T, Lou H. Dietary polyphenols and their biological significance. Int J Mol Sci 2007;8:950–88.

    • Crossref
    • Export Citation

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  • 1. Feillet-Coudray C, Sutra T, Fouret G, Ramos J, Wrutniak-Cabello C, Cabello G, et al. Oxidative stress in rats fed a high-fat high-sucrose diet and preventive effect of polyphenols: involvement of mitochondrial and NAD(P)H oxidase systems. Free Radic Biol Med 2009;46:624–32.

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  • 2. World Health Organization. Fact sheet: obesity and overweight. Internet: http://www.who.int/mediacentre/factsheets/fs311/en/ (Accessed January 2015).

  • 3. Unger RH. Lipid overload and overflow: metabolic trauma and the metabolic syndrome. Trends Endocrinol Metab TEM. 2003;14:398–403.

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  • 4. Yang ZH, Miyahara H, Takeo J, Katayama M. Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice. Diabetol Metab Syndr 2012;4:32.

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  • 5. Kainuma M, Fujimoto M, Sekiya N, Tsuneyama K, Cheng C, Takano Y, et al. Cholesterol-fed rabbit as a unique model of nonalcoholic, nonobese, non-insulin-resistant fatty liver disease with characteristic fibrosis. J Gastroenterol 2006;41:971–80.

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  • 6. McBride P. Triglycerides and risk for coronary artery disease. Curr Atheroscler Rep 2008;10:386–90.

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  • 7. Tajima N, Kurata H, Nakaya N, Mizuno K, Ohashi Y, Kushiro T, et al. Pravastatin reduces the risk for cardiovascular disease in Japanese hypercholesterolemic patients with impaired fasting glucose or diabetes: diabetes subanalysis of the Management of Elevated Cholesterol in the Primary Prevention Group of Adult Japanese (MEGA) study. Atherosclerosis 2008;199:455–62.

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  • 8. Unger RH, Orci L. Diseases of liporegulation: new perspective on obesity and related disorders. FASEB J Off Publ Fed Am Soc Exp Biol 2001;15:312–21.

  • 9. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 2004;114:1752–61.

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  • 10. Blokhina O, Virolainen E, Fagerstedt KV. Antioxidants, oxidative damage and oxygen deprivation stress: a review. Ann Bot 2003 Jan91. Spec No:179–94.

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  • 11. Wang X, Martindale JL, Liu Y, Holbrook NJ. The cellular response to oxidative stress: influences of mitogen-activated protein kinase signalling pathways on cell survival. Biochem J 1998;333:291–300.

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  • 12. Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev 2002;23:599–622.

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  • 13. Meydani M, Lipman RD, Han SN, Wu D, Beharka A, Martin KR, et al. The effect of long-term dietary supplementation with antioxidants. Ann N Y Acad Sci 1998;20:352–60.

  • 14. Saito M, Ueno M, Ogino S, Kubo K, Nagata J, Takeuchi M. High dose of Garcinia cambogia is effective in suppressing fat accumulation in developing male Zucker obese rats, but highly toxic to the testis. Food Chem Toxicol Int J Publ Br Ind Biol Res Assoc 2005;43:411–19.

    • Crossref
    • Export Citation
  • 15. Duke J, Bogenschutz-Godwin M, duCellier J, Duke PA. Handbook of medicinal herbs, 2nd ed. Boca Raton, FL: CRC Press, 2002:481.

  • 16. Chuah LO, Ho WY, Beh BK, Yeap SK. Updates on antiobesity effect of Garcinia Origin (-)-HCA. Evid Based Complement Altern Med ECAM 2013;doi: 10.1155/2013/751658.

  • 17. Dos Reis SB, de Oliveira CC, Acedo SC, Miranda DD, da C, Ribeiro ML, Pedrazzoli J, et al. Attenuation of colitis injury in rats using Garcinia cambogia extract. Phytother Res PTR 2009 Mar23:324–9.

    • Crossref
    • Export Citation
  • 18. Mahendran P, Vanisree AJ, Shyamala Devi CS. The antiulcer activity of Garcinia cambogia extract against indomethacin-induced gastric ulcer in rats. Phytother Res PTR 2002;16:80–3.

    • Crossref
    • Export Citation
  • 19. Oluyemi KA, Omotuyi IO, Jimoh OR, Adesanya OA, Saalu CL, Josiah SJ. Erythropoietic and anti-obesity effects of Garcinia cambogia (bitter kola) in Wistar rats. Biotechnol Appl Biochem 2007 Jan46:69–72.

    • Crossref
    • PubMed
    • Export Citation
  • 20. Hsu SC, Huang CJ. Reduced fat mass in rats fed a high oleic acid-rich safflower oil diet is associated with changes in expression of hepatic PPARalpha and adipose SREBP-1c-regulated genes. J Nutr 2006 Jul136:1779–85.

    • Crossref
    • PubMed
    • Export Citation
  • 21. Shivapriya S, Sandhiya S, Subhasree N, Aruna A, Dubey G. In vitro assessment of antibacterial and antioxidant activities of fruit rind extracts of Garcinia cambogia. L Int J Pharm Pharm Sci 2013;5:254–7.

  • 22. Harborne J. Phytochemical methods. New Delhi: Springer (India) Pvt. Ltd, 2005:17.

  • 23. Singleton VL, RossiJr JA. Colorimetry of total phenolics with phosphomolybdic-phosphotungstic acid reagents. AmJ Enol Vitic 1965;16:144–58.

  • 24. Velioglu YS, Mazza G, Gao L, Oomah BD, Activity A. Total phenolics in selected fruits, vegetables, and grain products. J Agric Food Chem 1998;46:4113–17.

    • Crossref
    • Export Citation
  • 25. Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: the FRAP assay. Anal Biochem 1996 Jul 15239:70–6.

    • Crossref
    • PubMed
    • Export Citation
  • 26. Beutler E, Duron O, Kelly BM. Improved method for the determination of blood glutathione. J Lab Clin Med 1963;61:882–8.

    • PubMed
    • Export Citation
  • 27. Wendel A. Glutathione peroxidase. Methods Enzymol 1981;77:325–33.

  • 28. Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121–6.

  • 29. Agarwal R, Chase SD. Rapid, fluorimetric-liquid chromatographic determination of malondialdehyde in biological samples. J Chromatogr B Analyt Technol Biomed Life Sci 2002;775:121–6.

    • Crossref
    • PubMed
    • Export Citation
  • 30. Sellamuthu PS, Arulselvan P, Kamalraj S, Fakurazi S, Kandasamy K. Protective nature of mangiferin on oxidative stress and antioxidant status in tissues of streptozotocin-induced diabetic rats. ISRN Pharmacology 2013;2013:750109 (10 pages).

    • PubMed
    • Export Citation
  • 31. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem 1951 Nov193:265–75.

    • PubMed
    • Export Citation
  • 32. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38:1103–11.

    • Crossref
    • PubMed
    • Export Citation
  • 33. Ahima RS. Digging deeper into obesity. J Clin Invest 2011;121:2076–9.

  • 34. Sripradha R, Magadi SG. Efficacy of garcinia cambogia on body weight, inflammation and glucose tolerance in high fat fed male wistar rats. J Clin Diagn Res JCDR. 2015 Feb;9(2):BF01–4.

    • Crossref
    • Export Citation
  • 35. Jang WS, Choung SY. Antiobesity effects of the ethanol extract of Laminaria japonica Areshoung in high-fat-diet-induced obese rat. Evid-Based Complement Altern Med ECAM 2013;2013:492807.

  • 36. Suchitra M, Kumar M, Bitla A, Rao A, Alok S. Atherogenic dyslipidemia in diabetic nephropathy: lipoprotein (a), lipid ratios and atherogenic index. Int J Res Med Sci 2013;1:455–9.

    • Crossref
    • Export Citation
  • 37. Sullivan AC, Triscari J, Hamilton JG, Miller ON, Wheatley VR. Effect of (-)-hydroxycitrate upon the accumulation of lipid in the rat. I Lipogenesis Lipids 1974;9:121–8.

  • 38. Tharachand IS. Mythili avadhani. Medicinal properties of Malabar Tamarind [Garcinia cambogia (Gaertn.) DESR. Int J Pharm Sci Rev Res 2013;19:101–7.

  • 39. Asha SK, Anila L, Vijayalakshmi NR. Flavonoids from Garcinia cambogia lower lipid levels in hypercholesterolemic rats. Food Chem 2001;72:289–94.

    • Crossref
    • Export Citation
  • 40. Peng Y, Rideout D, Rakita S, Lee J, Murr M. Diet-induced obesity associated with steatosis, oxidative stress, and inflammation in liver. Surg Obes Relat Dis Off J Am Soc Bariatr Surg 2012;8:73–81.

  • 41. Melov S. Mitochondrial oxidative stress. Physiologic consequences and potential for a role in aging. Ann N Y Acad Sci 2000;908:219–25.

    • PubMed
    • Export Citation
  • 42. Slatter DA, Bolton CH, Bailey AJ. The importance of lipid-derived malondialdehyde in diabetes mellitus. Diabetologia 2000;43:550–7.

    • Crossref
    • PubMed
    • Export Citation
  • 43. Meng R, Zhu D-L, Bi Y, Yang D-H, Wang Y-P. Anti-oxidative effect of apocynin on insulin resistance in high-fat diet mice. Ann Clin Lab Sci 2011;41:236–43.

    • PubMed
    • Export Citation
  • 44. Just MJ, Recio MC, Giner RM, Cuéllar MJ, Máñez S, Bilia AR, et al. Anti-inflammatory activity of unusual lupane saponins from Bupleurum fruticescens. Planta Med 1998;64:404–7.

    • Crossref
    • PubMed
    • Export Citation
  • 45. Ruch RJ, Cheng SJ, Klaunig JE. Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea. Carcinogenesis 1989;10:1003–8.

    • Crossref
    • PubMed
    • Export Citation
  • 46. Salah N, Miller NJ, Paganga G, Tijburg L, Bolwell GP, Rice-Evans C. Polyphenolic flavanols as scavengers of aqueous phase radicals and as chain-breaking antioxidants. Arch Biochem Biophys 1995;322:339–46.

    • Crossref
    • PubMed
    • Export Citation
  • 47. Han X, Shen T, Lou H. Dietary polyphenols and their biological significance. Int J Mol Sci 2007;8:950–88.

    • Crossref
    • Export Citation
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    Effect of Garcinia cambogia extract on high-fat-diet-induced dyslipidemia and oxidative stress.