Anti-diabetic and antioxidant effects of virgin coconut oil in alloxan induced diabetic male Sprague Dawley rats

doi:10.4236/jdm.2013.34034

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Vol.3, No.4, 221-226 (2013) Journal of Diabetes Mellitus

http://dx.doi.org/10.4236/jdm.2013.34034

Anti-diabetic and antioxidant effects of virgin

coconut oil in alloxan induced diabetic male

Sprague Dawley rats

Bolanle Iranloye1*, Gabriel Oludare1, Makinde Olubiyi1,2

1Department of Physiology, College of Medicine, University of Lagos, Lagos, Nigeria;

*Corresponding Author: [email protected]

2Department of Physiology, Kogi State University, Ayangba, Nigeria

Received 25 September 2013; revised 20 October 2013; accepted 28 October 2013

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

ABSTRACT

Oxidative stress has been discovered to be in-

volved in the progression of diabetes mellitus.

The antioxidant properties of virgin coconut oil

(VCO) among other functions might have a be-

neficial effect in ameliorating the disease. This

study w as aimed to determine the glycemic and

antioxidant effects of VCO in alloxan induced

diabetic rats. 24 male Sprague-Dawley rats w ere

divided into 4 group s as follows: control (C), dia-

betes untreated (DUT), diabetes treated with 7.5

ml/kg VCO (DT7.5) and diabetes treated with 10

ml/kg VCO (DT10). Alloxan (100 mg/kg b.w I.P)

was used to induce diabetes and VCO was ad-

ministered orally once daily for 4 w eeks. Fasting

blood glucose level w as measured on Day 0 (72

hours post alloxan injection) and after 4 weeks.

Glucose tolerance test was conducted on the

4th week as well as the determination of serum

insulin and liver antioxidant parameters using

standard biochemical methods. Values are means

± S.E.M., compared by ANOVA and Tukey’s post

hoc test. The result s show that VCO significantly

reduced the fasting blood glucose level in DT7.5

rats (132.4 ± 6.911) and DT10 rats (131.6 ± 12.2)

are compared with DUT rats (320.4 ± 22.99) and

improved the oral glucose tolerance. Serum in-

sulin was increased in DT10 rats. GSH activities

significantly increased p < 0.05 in DT10 rats (0.39

± 0.022) when compared to DUT rats (0.032 ±

0.004). CAT activities also significantly increased

p < 0.05 in DT7.5 (17.63 ± 0.61) and DT10 rats

(30.88 ± 0.97) w hen compared to DUT rats (10.98

± 0.6). SOD activities significantly increased p <

0.05 in DT7.5 (2.634 ± 0.04) and DT10 rats (2.258 ±

0.32) when compared to DUT rats (1.366 ± 0.05)

while MDA significantly reduced p < 0.05 in DT7.5

(49.16 ± 0.51) and DT10 (33.64 ± 0.42) rats when

compared to DUT rats (99.93 ± 4.79). This study

revealed that VCO has a hypoglycemic action,

enhances insulin secretion and also ameliorates

oxidative stress induced in type I (alloxan-in-

duced diabetic) male rats.

Keywords: Virgin Coconut Oil; Oxidative Stress;

Blood Glucose; Glucose Tolerance

1. INTRODUCTION

Diabetes mellitus characterized by hyperglycaemia, is

due to the deficiency of insulin secretion or its action. It

has been associated with a syndrome of disturbance in

the homeostasis of carbohydrate, fat and protein metabo-

lism [1]. Diabetes mellitus has been categorized into type

1 and type 2 diabetes. Type 1 diabetes refers to defi-

ciency of endogenous insulin which is caused by a cellu-

lar-mediated auto immune destruction of the beta cells in

the pancreas which produces insulin. And type 2 diabetes

is as a result of a decreased response to insulin by its

receptors, which is also referred to as insulin resistance

[1,2].

Oxidative stress contributes significantly to the patho-

physiology of several diseases which include diabetes

[3]. Alloxan, a chemical used in inducing diabetes acts

mainly by the generation of reactive oxygen species

(ROS) [3]. It preferentially accumulates in the GLUT2

glucose transporter in the pancreatic beta cells and sub-

sequently leads to the death of the cells. Therefore al-

loxan is a model compound when studying diabetes as a

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226

222

result of ROS mediated beta cell toxicity.

Historically, coconut oil has been renowned for its

medicinal and nutritional value. Studies on the biological

effects of coconut oil have proven that it ameliorates

oxidative stress by boosting the antioxidant defense sys-

tem, mopping up free radicals and reducing lipid peroxi-

dation [4,5]. It has also been reported to suppress micro-

bial and viral activities [6], promote weight loss and en-

hance thyroid function [7]. Other researches have also re-

ported that coconut oil possesses anti-inflammatory and

anti-ulcerogenic effect [8], while also having the ability

to increase the level of high density lipoprotein (HDL)

cholesterol and to reduce the level of low density lipo-

protein (LDL) in serum and tissues [4].

Copra oil and virgin coconut oil (VCO) are the two

main types of coconut oil. Copra oil is extracted from the

dried endosperm of the coconut fruit while VCO is pro-

duced by a “wet” extraction process from the fresh en-

dosperm of the coconut fruit [9]. The mode of extraction

of VCO makes it more beneficial than copra oil. This is

because no chemicals are used and there is little or no

application of heat during its extraction. Therefore it re-

tains more of the natural active components which in-

clude polyphenols which have been proven to boost the

antioxidant defense system [4].

The present study therefore, determined the possible

role of the antioxidant effect of VCO on oxidation/per-

oxidation linked with diabetes mellitus in alloxan in-

duced diabetic rats as well as its possible effect on glu-

cose homeostasis.

2. MATERIALS AND METHODS

2.1. Animals

Male Sprague-Dawley rats weighing 120 - 150 g were

obtained from the Laboratory Animal House of the Col-

lege of Medicine of the University of Lagos. The rats

were allowed to acclimatize for two weeks before the

commencement of the experiment and were fed with

standard rat chow and water ad libitum at 20˚C - 25˚C

under a 12 h light/dark cycle. All animal handling and

experiment protocols complied with the international

guidelines for laboratory animals as supported by the

College of Medicine of the University of Lagos ethical

committee.

2.2. Experimental Groups

Rats were randomly divided into 4 groups (n = 6):

Group 1, control (C) received 0.5 ml distilled water;

Group 2, diabetic untreated (DUT); Group 3, diabetic

treated with 7.5 ml/kg body weight of VCO (DT7.5) and

Group 4, diabetic treated with 10 ml/kg body weight of

VCO (DT10). Seventy two hours following the induction

of diabetes, VCO was administered orally for 4 weeks

daily at the appropriate dose for Groups 3 and 4 animals.

2.3. Induction of Diabetes

Following 2 weeks acclimatization of the rats, Alloxan

monohydrate (manufactured by Denixco Private limited,

India) was used to induce type 1 diabetes in Groups 2, 3

and 4. A dose of 100 mg/kg body weight of Alloxan

monohydrate was administered only once intraperito-

neally. A mild pressure was applied at the spot of injec-

tion to enhance absorption. After 3 days of administra-

tion the fasting blood glucose level of these rats were

measured. Rats with fasting blood glucose level above

200 mg/dl were considered diabetic.

2.4. Measurement of Blood Glucose

Blood glucose level was measured using One Touch

Ultra test strips (Lifescan Inc. Milpitas, USA). Blood

was obtained from the rats at the tip of rat’s tail. The

blood was dropped on the test strips already inserted in a

One Touch Ultra Easy Glucometer (Lifescan Inc.

Milpitas, USA). The glucose levels of the animal were

displayed on the glucometer in about 5 seconds. Blood

glucose level was measured at the beginning of the ex-

periment and after 4 weeks.

2.5. Preparation of Virgin Coconut Oil

Mature coconuts were bought from Mushin Market,

Lagos, Nigeria. VCO was extracted using the wet extrac-

tion method [4]. The solid endosperm of mature coconut

was crushed and made into thick slurry. About 500 ml of

water was added to the slurry obtained and squeezed

through a fine sieve to obtain coconut milk. The resultant

coconut milk was left for about 24 hours to facilitate the

gravitational separation of the emulsion. Demulsification

produced layers of an aqueous phase (water) on the bot-

tom, an emulsion phase (cream) in the middle layer and

an oil phase on top. The oil on top was scooped and

warmed for about 3 minutes to remove moisture. The

obtained oil was then filtered and stored at room tem-

perature.

2.6. Oral Glucose Tolerance Test (OGTT)

On the 4th week of the experiment, all groups were

subjected to oral glucose tolerance test (OGTT). The rats

were fasted overnight for sixteen-hour (16-h) and subse-

quently challenged with a glucose load of 2 ug/kg body

weight. Blood glucose levels were determined at 0 h

(pre-glucose treatment) and at 30, 60, 90, 120 and 180

min (post glucose treatment). The glucose levels were

measured using a complete blood glucose monitoring

system (One-Touch Ultra Easy Glucose Meter, Lifescan

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226 223

Inc. Milpitas, USA).

2.7. Sample Collection

The rats were anesthetized by intramuscular injection

of 50 mg/kg of ketamine. The liver was removed and

homogenized in phosphate buffer, pH 7.4 and stored at

−20˚C. Blood samples were also collected from the ven-

tricle of the heart, allowed to clot and spun at 3000 rmp

to obtain serum sample for insulin assay.

2.8. MDA L evel

As a marker of lipid peroxidation, the level of malon-

dialdehyde (MDA) in the liver homogenate was meas-

ured [10]. 1 ml of the tissue homogenate was thoroughly

mixed with 2 ml of TCA-TBA-HCl solution and heated

for 15 minutes in a water bath. After cooling, the pre-

cipitate is removed by centrifugation and the absorbance

measured at 535 nm is taken as an index of lipid peroxi-

dation.

2.9. SOD, CAT and GSH Activities

At the end of the 4 week period of the experiment, the

activity of the superoxide dismutase (SOD) enzyme in

the liver homogenate was determined [11]. The reaction

was carried out in 0.5m sodium carbonate buffer pH 10.2

and was initiated by the addition of 3 × 10−4 epinephrine

in 0.005 N HCl. The absorbance was read at 320 nm.

Catalase (CAT) activity was determined by measuring

the exponential disappearance of H2O2 at 240 nm and

expressed in units/mg of protein [12]. Reduced glu-

tathione (GSH) content of the liver homogenate was de-

termined [13], based on the reaction of Ellman’s reagent

5,5’dithiobis-2-nitrobenzoic acid (DNTB) with the thiol

group of GSH at pH 8.0 to produce 5-thiol-2-nitroben-

zoate which is yellow at 412 nm. Absorbance was re-

corded using UV-Visible Spectrophotometer in all meas-

urement. The protein concentrations of the samples were

measured using the method of Bradford [14].

2.10. Serum Insulin Level

Enzyme-Linked Immunosorbent Assay (ELISA) was

used to measure the level of insulin in the serum sample

obtained from the animal. The protocol used was as de-

scribed by the manufacturer of the assay kit (Enzo-Life

Science).

2.11. Statistical Analysis

Data were presented as mean and Standard Error of

Mean (SEM). One-way ANOVA and Tukey’s post hoc

test was used to determine the specific pairs of groups

that were statistically different at p < 0.05. Analysis was

performed with GraphPad software.

3. RESULTS

3.1. Fasting Blood Glucose

Fasting blood glucose was measured at 72 hours post

alloxan injection. Hyperglycemia was observed in DUT,

DT7.5, and DT10 rats. After four weeks of coconut oil

treatment, DT7.5 and DT10 rats showed a significant re-

duction (p < 0.05) in fasting blood glucose level com-

pared with DUT rats (Figures 1 and 2).

3.2. Oral Glucose Tolerance Test (OGTT)

After 4 weeks administration of coconut oil, glucose

concentration (pre glucose challenge) in both DT7.5 and

DT10 rats showed a significantly reduced glucose con-

centration when compared with DUT rats. As expected,

there was an initial increase in blood glucose 30 minutes

post glucose challenge which reduced over time as pre-

sented in Figure 2. Three hours post glucose challenge

showed that DT7.5 and DT10 significantly reduced blood

glucose level when compared with DUT rats. The effect

Figure 1. Fasting blood glucose level (mg/dl) of diabetic rats

induced with alloxan. Values are expressed as mean ± S.E.M.

*p < 0.05 is significant compared with Group 1 (control).

Figure 2. Effect of 4 weeks VCO supplementation on fasting

blood glucose level (mg/dl) in alloxan induced diabetic rats.

Values are expressed as mean ± S.E.M. *p < 0.05 is significant

compared with Group 1 (control). #p < 0.05 is significant com-

pared with Group 2 (diabetes untreated).

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226

224

of DT10 was more effective than that of DT7.5 (Figure 3). antioxidative defence capacity, thus the generation of

ROS by alloxan leads to the death of these cells. This is

possible due to the reduction product of the reaction,

dialuric acid, which generates hydrogen peroxide, su-

peroxide radicals and hydroxyl radicals. These radicals

are responsible for the death of the beta cells and the

ensuing state of insulin-dependent alloxan diabetes [3].

3.3. Antioxidant Enzymes Activities and

MDA Levels

MDA level was significantly increased in DUT rats

when compared to control (p < 0.05), however, MDA

levels were significantly reduced in DT7.5 and DT10 rats

compared with DUT rats. Though a significant reduction

in DT7.5 rats was observed when compared with DUT

rats, the value observed compared with the control still

shows lipid peroxidation (Table 1). In the antioxidant

enzymes, SOD activity was significantly reduced in DUT

rats when compared with control. DT7.5 and DT10 sig-

nificantly increased the activity of SOD when compared

with DUT rats. The enhancement in SOD activity how-

ever was still significantly lower compared with the con-

trol values. The activity of GSH was significantly re-

duced in DUT rats when compared with control. How-

ever, DT10 rats significantly increased the activity of

GSH while DT7.5 had no effect on the activity of GSH

when compared with DUT rats. Lastly, CAT activity was

reduced in DUT treated rats when compared with control

rats. DT7.5 and DT10 significantly increased the activity

of CAT when compared with DUT rats. DT10 enhanced

this activity more than the control rats while this activity

was still decreased in DT7.5 rats compared to control rats

(Table 1).

This study reports marked hyperglycemia 72 hours

post alloxan injection (100 mg/kg body weight). This is

supported by other previous studies and reports [15-17].

Four weeks of treatment with VCO decreased the fasting

blood glucose level in DT7.5 and DT10 rats when com-

pared with DUT rats. Supporting the report that coconut

oil has a hypoglycemic effect [18,19]. Since, alloxan

generates ROS to impair the beta cell function; it is pos-

sible that VCO alleviates blood glucose level due to its

antioxidant property. It is possible that the beta cells re-

sponse to oxidative stress might have been enhanced thus

enabling the cells to carry out their function of insulin

production. Consequently, this increase in insulin pro-

duction will lead to reduced blood glucose.

Oral glucose tolerance test is used to measure insulin

function or the degree of peripheral utilization of glucose

[20]. In this study, following glucose administration,

there was a minimal rise in the blood glucose level which

fell below the control value after 2 hours in the control

rats. In DUT, DT7.5 and DT10 rats there was a marked rise

in blood glucose level after the glucose challenge and the

blood glucose level failed to return to the control value

3.4. Serum Insulin Level

Table 2 shows the serum insulin level of male rats

treated with VCO. DUT rats shows a significantly re-

duced insulin level when compared control. DT10 alone

significantly increased the level of insulin when com-

pared with DUT rats. Though the values of DT7.5 were

increased it was however not significant and the values

obtained was still significantly lower than those of the

control rats.

4. DISCUSSION

Figure 3. Effect of virgin coconut oil (VCO) on oral glucose

tolerance test (OGTT). Values are expressed as mean ± S.E.M.

*p < 0.05 is significant compared with Group 1 (control). #p <

0.05 is significant compared with Group 2 (diabetes untreated).

Alloxan, used in inducing diabetes is a toxic glucose

analogue that generates ROS in the presence of intracel-

lular thiols [3]. The beta cells of the pancreas have a low

Table 1. Effect of VCO on the activity of superoxide dismutase, glutathione, catalase and malondialdehyde levels.

Control (C)Diabetes untreated (DUT)Diabetes + 7.5 ml/kg VCO (DT7.5) Diabetes + 10 ml/kg VCO (DT10)

MDA (U/mg protein) 31.78 ± 2.1899.93 ± 4.79* 49.16 ± 0.51*# 33.64 ± 0.42#

SOD (U/mg protein) 3.91 ± 0.14 1.37 ± 0.05* 2.63 ± 0.04*# 2.26 ± 0.32*#

GSH (U/mg protein) 0.11 ± 0.0070.03 ± 0.004* 0.04 ± 0.008* 0.39 ± 0.022*#

CAT (U/mg protein) 25.87 ± 0.9610.98 ± 0.60* 17.63 ± 0.61*# 30.88 ± 0.97*#

alues are expressed as mean ± S.E.M. *p < 0.05 is significant compared with control. #p < 0.05 is significant compared with diabetes untreated group.

OPEN ACCESS

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226 225

Table 2. Effect of virgin coconut oil (VCO) on serum insulin

level.

Insulin level (μiu/ml)

Control (C) 3.05 ± 0.25

Diabetes untreated (DUT) 1.19 ± 0.04*

Diabetes + 7.5 ml/kg VCO (DT7.5) 1.90 ± 0.40*

Diabetes + 10 ml/kg VCO (DT10) 2.50 ± 0.03#

Values are expressed as mean ± S.E.M. *p < 0.05 is significant compared

with Control. #p < 0.05 is significant compared with Diabetes untreated

group.

even after 3 hours indicating impairment in glucose tol-

erance which is an indication of diabetes. In DT7.5 and

DT10 rats there was a significant improvement in glucose

tolerance compared with the DUT rats, supporting the

view that ingestion of VCO improves glucose tolerance

in diabetic rats [21]. In addition, the 10 ml/kg dosage of

VCO proved to have a greater effect as the blood glucose

level in DT10 rats after 3 hours of glucose challenge was

closer to the control value than in DT7.5 rats.

It has been reported that the lauric oil in VCO pos-

sesses insulino-tropic properties [18]. Serum insulin was

increased in DT10 rats with a non significant increase in

DT7.5 rats compared with DUT rats. Since the dosage of

7.5 ml/kg body weight of VCO could not elevate serum

insulin, it implies that the 10 ml/kg body weight dose is

more effective in the control of glucose homeostasis than

the 7.5 ml/kg body weight. This is evidenced by the re-

duction in blood glucose level and the improvement in

glucose tolerance compared to DUT rats as discussed

earlier.

Antioxidant enzymes are critical part of cellular pro-

tection against reactive oxygen species and ultimately

oxidative stress. Oxidative stress is determined by the

balance between the generation of ROS such as super-

oxide anion (2

O) and the antioxidant defense systems

such as superoxide dismutase (SOD). Antioxidants en-

zymes involved in the elimination of ROS include SOD,

CAT and GSH, respectively. The present study showed a

decrease in the activity of all measured antioxidants en-

zymes in DUT rats. This indicates a decrease in the anti-

oxidant defense system. However treatment with VCO in

DT7.5 and DT10 rats increased the activities of the anti-

oxidant enzymes. Since oxidative stress contributes sig-

nificantly to the pathophysiology of diabetes [22], sub-

stances that suppress oxidative stress might be therapeu-

tically beneficial. Studies have shown that exogenously

administered antioxidants have protective effects on dia-

betes, thus providing insight into the relationship be-

tween free radicals and diabetes [20,22-24]. The reduc-

tion in fasting blood glucose of rats treated with VCO

after 4 weeks and a decrease in the OGTT of the rats

compared with the diabetic untreated rats can be associ-

ated to the antioxidant effect of VCO.



5. CONCLUSION

VCO alleviates hyperglycemia and improves glucose

tolerance probably by its antioxidant effect which con-

sequently leads to improvement of insulin secretion as

examined in this study. The study also shows that a dos-

age of 10 ml/kg body weight of VCO is quite beneficial

and more effective than that of 7.5 ml/kg body weight.

This was evident because the 7.5 ml/kg body weight did

not increase insulin secretion and possibly because of the

higher OGTT values.

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